For this first issue of 2026, we delve specifically into healthy hematopoiesis, from the most immature stem cells to more committed progenitors. We are also excited to showcase no less than 3 preprints directly submitted by the Simply Blood community! If you want to see your most recent preprint highlighted here, submit it using this link.

From the Simply Blood Community:

DNMT3A-R882 mutations intrinsically drive dysfunctional neutropoiesis from human haematopoietic stem cells

https://www.biorxiv.org/content/10.1101/2025.10.08.679225v1

Via single-cell and multi-omic profiling of DNMT3A-R882 CH (Clonal Haematopoiesis), we revealed that the mutation drives fast and abundant human HSCs differentiation into dysfunctional neutrophils. Our findings, validated in humanised mice, identify aberrant DNMT3A-R882 HSC-driven neutropoiesis as a key link between CH, immune dysregulation and risk of inflammatory disease.

Social media handles: @GiovannaMantica (Twitter)

Chromatin Accessibility Shapes Developmental-Specific Lineage Plasticity in Hematopoiesis

https://doi.org/10.64898/2025.12.02.691283

We present a chromatin accessibility map of human first trimester HSPCs and compare fetal and adult cell states.
In brief:
- the early fetal HSC state is low-primed and permissive, reflected in vitro by mixed lineage output from single HSCs, as opposed to more myeloid-primed and functionally biased adult HSCs.
- lympho-myeloid priming in fetal lymphoid cell state compared to more distinct lymphoid in adult
- reduced B-lymphoid commitment at the chromatin level in fetal lymphoid progenitors,

Enhanced lineage plasticity during fetal life may underlie the prenatal susceptibility to mutational drivers of acute lymphoblastic leukemia.

Contact address: charlotta.boiers@med.lu.se
Social media handles: LinkedIn (Charlotta Böiers); @boierslab.bsky.social

The ratio of RUNX1-ETO oncoprotein to normal RUNX1 expression determines the balance between endothelial reprogramming and hematopoietic cell growth

https://www.biorxiv.org/content/10.64898/2025.12.19.695648v1

In t(8;21) acute myeloid leukemia (AML) the RUNX1 DNA binding domain is fused to the RUNX1T1 protein producing the RUNX1-ETO onco-fusion protein. We previously showed that t(8;21) leukemic stem cells aberrantly activate endothelial signalling pathways to initiate blast cell proliferation. Here, we employed a human embryonic stem cell (ESC) line expressing an inducible RUNX1-ETO transgene to determine whether RUNX1-ETO directly induces endothelial signalling pathways or whether it is dependent on AML progression. Using single cell analyses we show that RUNX1-ETO induction reprograms ESC-derived myeloid progenitors towards endothelial cells. Integrated data analysis demonstrates (i) that endothelial reprogramming is RUNX1-ETO concentration-dependent and irreversible, (ii) that when RUNX1-ETO and RUNX1 expression levels are equal, a sub-population of blood progenitors escapes reprogramming and (iii) keeps proliferating when co-cultured with endothelial cells. Our experiments provide important insights into the earliest stages of epigenetic reprogramming by oncogenic transcription factors in AML.

Contact address: constanze.bonifer@mcri.edu.au

Hematopoiesis

Hematopoietic proliferation is orchestrated by the sequential and lineage-specific activation of Cyclin D, Cyclin E and CDKN sub-modules within the G1/S network

https://www.biorxiv.org/content/10.1101/2025.05.15.654268v1

Here, the authors show that coordination between the G1/S cell-cycle network and developmental programs shapes proliferation and differentiation across human hematopoietic cell types. By integrating single-cell transcriptomics with mathematical modeling, they identify cyclin D– and cyclin E–centered submodules whose variable expression creates distinct routes from G1 to S phase. These divergent trajectories explain why hematopoietic stem and progenitor populations display different proliferative behaviors despite sharing the same microenvironment. The model maps 68 hematopoietic cell types to specific G1/S parameter sets, linking cell-cycle dynamics to lineage bias.

In vivo CRISPR screening identifies SAGA complex members as key regulators of hematopoiesis

https://www.biorxiv.org/content/10.1101/2022.07.22.501030v2

Researchers report that genome-wide in vivo CRISPR knockout screens in HSCs identify the SAGA complex—particularly Tada2b and Taf5l—as essential regulators of hematopoiesis. Loss of these components severely impaired blood production, caused accumulation of immature cells in the bone marrow, and activated interferon-related pathways. In a human MDS model, depletion of the same factors heightened aberrant cell expansion and inflammatory signaling, suggesting that reduced SAGA activity may contribute to disease progression.

Differences between in vivo and ex vivo hematopoietic model systems modulate the outcomes of genetic perturbations

https://www.biorxiv.org/content/10.1101/2025.09.02.673692v1

Using Perturb-seq on hematopoietic progenitors grown in vivo and ex vivo, the authors show that baseline transcriptional shifts—lower interferon programs and higher growth/metabolic activity—partly explain why KO effects diverge between model systems, a result validated in independent splenic KO data. These baseline differences predict some divergence in KO effects, highlighting the need to improve both culture systems and computational prediction approaches.

Differentiation stage-specific use of cap-independent and cap-dependent translation initiation in hematopoiesis

https://www.biorxiv.org/content/10.1101/2025.09.24.678136v1

Using a newly generated IRES/Cap reporter mouse, the study reveals that while caloric stress increases IRES/Cap as expected, IRES/Cap also rises progressively during hematopoietic and epithelial differentiation under homeostasis, independent of protein output or cell cycle. Across tissues, cells with lower relative-IRES utilization show markedly higher multipotent potential, and PTBP1 emerges as a key mediator of this shift. Together, these findings identify low IRES/Cap as a stemness signature and implicate translation-initiation preferences in differentiation.

Trimodal Single-Cell Gene Regulatory Networks Reveal Principles of Stemness Loss and Cell Fate Acquisition in Human Hematopoiesis

https://www.biorxiv.org/content/10.1101/2025.09.11.675740v1

The study establishes the first dynamic enhancer-based gene regulatory networks (eGRNs) to resolve early human hematopoietic fate decisions. Using high-resolution TEA-seq–derived trajectories anchored to defined immunophenotypic populations, the work shows that stemness loss occurs gradually through reduced transcription factor abundance well before chromatin closure, whereas lineage identity emerges stepwise via enhancer reconfiguration and activation of lineage-specific eGRNs. These dynamics generate discrete regulatory states that align with known populations, reconciling continuous and discrete models of hematopoiesis. The authors also provide an interactive resource enabling exploration of eGRNs and developmental trajectories.

Clonal memory of cell division in humans diverges between healthy haematopoiesis and acute myeloid leukaemia

https://www.biorxiv.org/content/10.1101/2025.06.24.660535v1

The study uses high-resolution ex vivo lineage–division tracking to reveal that human HSPCs inherit both division synchronicity and fate-commitment tendencies across at least two generations, demonstrating robust clonal memory. These coupled memories persist across commitment stages and culture conditions, whereas leukemic HSPCs show markedly reduced synchronicity, indicating disrupted clonal memory in malignancy. Epigenetic remodeling with a bromodomain inhibitor partially restores division-related memory in leukemic cells, underscoring the plasticity of this trait. Together, the work positions clonal memory as a modifiable regulator of heterogeneity in healthy and malignant haematopoiesis.

The hidden predictors of human haematopoietic clonal fate

https://www.biorxiv.org/content/10.1101/2025.07.28.667115v1

The study introduces a human hematopoietic ex vivo experimental setup that supports differentiation into 15 lineages and enables longitudinal tracking of barcoded HSPC clones. By integrating single-cell transcriptomes, surface phenotypes, and clonal outputs, machine-learning models identify clonal fate modules that predict lineage commitment and uncover previously hidden correlates of multipotency. Among these, CD200 marks a subset of HSCs with broad output potential, a feature exploited to enhance the purity of manufactured type I dendritic cells for immunotherapy. This framework refines the decoding of clonal fate in human HSPCs and highlights molecular signatures that distinguish truly multipotent clones.

Circulating hemocytes continue to proliferate throughout lifespan in Daphnia

https://www.biorxiv.org/content/10.1101/2025.10.07.680988v1

In Daphnia magna, circulating hemocytes continue to proliferate throughout adulthood, as shown by EdU incorporation, independent of molting or ovary cycle phase and only slightly declining with age. No evidence of de novo DNA synthesis was observed in other tissues, suggesting that hemocytes themselves constitute a self-renewing population rather than arising from a dedicated hematopoietic stem cell niche. While most hemocytes displayed a ploidy around 4, EdU-positive cells were enriched in S-phase, indicating active DNA replication. These findings reveal that hemocytes maintain mitotic activity throughout life, though it remains unclear whether proliferation balances cell loss or involves a distinct mitotically active subpopulation.

Disruption of hemocyte differentiation and distribution in Drosophila Ptr23c mutants

https://www.biorxiv.org/content/10.1101/2025.07.03.662979v1

The authors investigated the role of Ptr In Drosophila embryonic hemocyte development. Ptr23c null mutants did not alter total hemocyte number, apoptosis, or mitosis, but exhibited disrupted spatial distribution and accelerated differentiation at stage 12. Paradoxically, by stage 16, mature hemocytes were reduced by 50%, indicating premature maturation depletes the pool. 

A single-cell cytokine dictionary of human peripheral blood

https://www.biorxiv.org/content/10.64898/2025.12.12.693897v1

In this work, the authors present the Human Cytokine Dictionary, a comprehensive resource mapping cytokine responses across human immune cells. Using single-cell transcriptomics of nearly 10 million PBMCs from 12 donors stimulated with 90 cytokines, they reveal both donor-specific variations and robust consensus signatures. The dictionary enables interpretation of cytokine-driven responses in health and disease, including autoimmune and cancer contexts, and provides an open-access platform to guide therapeutic discovery.

The extent of myeloid skewing in blood is a biomarker of biological aging in mice and humans

https://www.biorxiv.org/content/10.64898/2026.01.20.700344v1

From the authors: The extent of myeloid skewing in aged mice correlates to an increased hematological and epigenetic age and increased disease burden. The extent of myeloid skewing in older adults is associated with an increased hazard ratio of mortality and correlates with higher frailty and inflammatory markers.

Hematopoietic stem cell

ATP2B1 expression identifies human hematopoietic stem cells across ontogeny with superior repopulation and self-renewal capacity

https://www.biorxiv.org/content/10.1101/2025.06.11.659017v1

In this study, the authors identify ATP2B1 (PMCA1) as a novel surface marker that resolves functional heterogeneity within human CD49f⁺ long-term hematopoietic stem cells (LT-HSCs) across ontogeny. CD49f⁺ATP2B1⁺ LT-HSCs from fetal liver, cord blood, and adult peripheral blood show substantially greater self-renewal and long-term repopulation capacity than ATP2B1⁻ cells. Multiomic profiling reveals enrichment of a TFEB–endolysosomal self-renewal program in ATP2B1⁺ LT-HSCs.

Human length telomeres restrict the regenerative potential of hematopoietic stem cells in mice 

https://www.biorxiv.org/content/10.1101/2025.08.26.672314v1

Using a mouse model with human-length telomeres (Telomice), the authors tested how extreme telomere shortening impacted hematopoiesis. Telomice maintain normal blood production at baseline, but repeated 5-FU injury or transplantation exposes a sharp depletion of bone marrow progenitors. The authors link this vulnerability to an accumulation of ultrashort telomeres undetectable by FISH, revealing how critically short telomeres drive bone marrow failure under stress.

MYD88 mutations in clonal hematopoiesis promote inflammation and hematopoietic stem cell expansion

https://www.biorxiv.org/content/10.1101/2025.06.19.660202v2

The study identified MYD88 mutations—including lymphoma-associated and novel variants—in CHIP (Clonal Hematopoiesis of Indeterminate Potential) among the general population and solid cancer patients. These mutations act as gain-of-function alleles in HSPCs, activating NF-κB and promoting a competitive fitness advantage. In mice, Myd88L252P drives myeloid bias, inflammation, and expansion of specific HSPC and immune cell clusters. An IRAK1/4 inhibitor blocks MYD88-dependent NF-κB signaling and reverses mutant cell expansion, establishing MYD88 as a rare CHIP driver acting through innate immune activation.

An Inflammatory and Quiescent HSC Subpopulation Expands with Age in Humans

https://www.biorxiv.org/content/10.1101/2025.09.01.673389v1

The authors generate a unified map of human HSC aging by integrating seven single-cell datasets. This work reveals previously unrecognized heterogeneity within the HSC compartment and uncovers a gene expression program linking inflammatory pathway activation with quiescence. An inflammatory HSC subpopulation enriched for this program increases with age

Polymer-based culture system enables expansion of human haematopoietic stem and progenitor cells while preserving ageing-associated transcriptional programs

https://www.biorxiv.org/content/10.1101/2025.09.10.675303v1

In this study, the authors assess a polymer-based ex vivo culture platform for modelling ageing human haematopoiesis. Using CD34⁺ cells from donors across age groups, the system supports robust HSPC expansion while maintaining age-associated transcriptional programs, including inflammatory signatures in cells from older individuals. Single-cell RNA sequencing confirms stable enrichment of key progenitor populations with conserved identities.

JAK2 signalling to HNRNPA1 represses retrotransposon activity in haematopoietic stem cells

https://www.biorxiv.org/content/10.1101/2025.07.07.663405v1

The authors map somatic retrotransposition in adult haematopoietic stem cells and uncover a previously unrecognised regulatory pathway. They show that cytokine-driven JAK2 activation, either via thrombopoietin or gain-of-function mutations, induces tyrosine phosphorylation of HNRNPA1, which in turn suppresses ERV, LINE and SINE expression and limits insertional mutagenesis, revealing a dynamic mechanism that links cytokine signalling and RNA-modulating HNRNP complexes to retrotransposon repression.

Functional Comparison to Ezh2 Reveals PRC2-Independent Functions of Jarid2 in Hematopoietic Stem Cell Lineage Commitment

https://www.biorxiv.org/content/10.1101/2025.07.18.665536v1

Researchers revisited the role of the PRC2 co-factor Jarid2 and uncovered evidence that its functions in hematopoiesis extend beyond canonical PRC2 activity. Comparing Jarid2- and Ezh2-deficient stem and progenitor cells revealed sharply divergent phenotypes: Ezh2 loss skewed differentiation toward myeloid and lymphoid-biased states, while Jarid2 loss selectively boosted T-cell output. Single-cell transcriptomics and functional assays showed that Ezh2 deficiency causes a block at the pre-pro-B stage, whereas Jarid2 deficiency leaves progenitors broadly intact. The contrasting outcomes point to a non-canonical role for Jarid2 in regulating lineage commitment.

Loss of cell cycle gatekeeping by CNOT3 impairs hematopoietic stem and progenitor cell division and repopulating activity

https://www.biorxiv.org/content/10.1101/2025.10.23.684176v1

This work describes the role of CNOT3, a core component of the CCR4–NOT complex, as a key post-transcriptional regulator of adult hematopoietic stem cell function. Conditional deletion of Cnot3 in mice triggered anemia, reduced bone marrow cellularity, splenic extramedullary hematopoiesis, and a transient expansion of immunophenotypic HSCs followed by their collapse. Transplantation assays and single-cell RNA sequencing showed that Cnot3-deficient HSPCs fail to sustain hematopoiesis and exhibit broad disruptions in lineage development.

ERAD Activity Distinguishes the Functional Heterogeneity of Hematopoietic Stem Cells

https://www.biorxiv.org/content/10.64898/2025.12.01.691501v1

Using a dual-fluorescence reporter system, this work reveals that endoplasmic-reticulum–associated degradation (ERAD) activity can prospectively predict the long-term reconstitution potential of individual hematopoietic stem cells. The authors found that ERAD states persist through self-renewal, pointing to an inheritable “proteostatic memory” that stratifies functional diversity within the HSC pool. Mechanistic analyses identified a SOCS2–JAK2–ERAD axis in which SOCS2 restrains JAK2 signaling to preserve ERAD function, while hyperactive JAK2 disrupts misfolded-protein clearance via interactions with Hrd1 and VCP. The results establish intrinsic proteostatic state as a heritable marker of HSC quality and a driver of stem cell heterogeneity.

Proteostasis Remodeling Across Development Defines Fetal, Neonatal, and Adult Hematopoietic Stem Cell States

https://www.biorxiv.org/content/10.64898/2025.12.12.694052v1

Researchers reveal that hematopoietic stem cells (HSCs) employ stage-specific proteostasis programs that differ markedly between fetal, neonatal, and adult stages. Quantitative in vivo analyses show a decoupling of protein synthesis and quality control during development, with early-life HSCs balancing high protein production and increased unfolded protein stress via specialized stress-buffering and degradation pathways. These pathways are largely dispensable in young adult HSCs but are critical for early HSC function and long-term fitness.

Differential sensitivity to LINE 1-induced damage contributes to the expansion of Tet2-deficient HSCs upon chronic inflammatory stress

https://www.biorxiv.org/content/10.1101/2025.07.21.665900v2

The authors here demonstrate that chronic inflammation impairs hematopoietic stem cell (HSC) function through derepression of recent LINE-1 (L1) transposable elements. In wild-type HSCs, prolonged low-dose LPS exposure reduces H3K9me3 at L1s, triggering L1 activation, DNA damage, and diminished clonogenic potential. Tet2-deficient HSCs resist this L1 derepression, gaining a competitive advantage under inflammatory conditions. 

Plcl1 Regulates Hematopoietic Stem Cell Function During Aging and Stress by Modulating Calcium Dynamics

https://www.biorxiv.org/content/10.1101/2025.09.15.674672v1

This work describes phospholipase C-like 1 (Plcl1) as a key regulator of intracellular calcium in quiescent hematopoietic stem cells (HSCs). Plcl1 deficiency lowers basal calcium, shifts the HSC pool toward CD41⁺ subsets, and activates a thrombopoietic bypass pathway under acute stress, enhancing platelet rebound and non-canonical megakaryocyte progenitor expansion. In aged HSCs, loss of Plcl1 exacerbates pool expansion, myeloid skewing, and impaired reconstitution, accompanied by reduced induction of calcium-responsive genes.

Impaired IL-10 Receptor Signaling Leads to Inflammation Induced Exhaustion in Hematopoietic Stem Cells

https://www.biorxiv.org/content/10.1101/2025.09.30.679613v1

From the authors: Wadley et al. show that IL-10 receptor signaling restrains inflammation-induced hematopoietic stem cell cycling and exhaustion; its blockade prolongs cycling, accelerates aging-related decline, and selectively favors Jak2V617F mutant HSCs, establishing IL-10 signaling as a critical regulator of inflammatory HSC exhaustion and malignant clonal evolution.

Developmental programming of hematopoietic stem cell dormancy by evasion of Notch signaling

https://www.biorxiv.org/content/10.64898/2026.01.02.697352v1

This work shows that dormant hematopoietic stem cells (HSCs) are established during embryogenesis rather than exclusively after birth. These low-dividing fetal HSCs evade Notch signaling within the fetal liver niche, entering a durable dormancy program that persists into adulthood. Temporally restricted perturbation of Notch signaling reveals a narrow window during development when reduced Notch exposure promotes quiescence and enhances long-term repopulation.

Megakaryopoiesis

Induction of Moderate DNA Damage Enhances Megakaryopoiesis and Platelet Production

https://www.biorxiv.org/content/10.1101/2025.05.08.652525v2

From the authors: Treatment of mice with low dose PARP inhibitors or gamma-irradiation enhances platelet counts. Low dose PARP inhibitor treatment leads to increased DNA damage in MKs and MK progenitors and enhances bone marrow megakaryopoiesis.

Turbulence orchestrates actin-mitochondria dynamics to preserve GPIbα and support iPSC-derived platelet biogenesis

https://www.biorxiv.org/content/10.1101/2025.05.22.655481v2

In this work the authors describe a turbulence-assisted system, which enhances the production of iPSC-derived platelets from immortalized megakaryocyte progenitors, improving yield and functionality. Functional GPIbα⁺ platelets retain mitochondrial integrity, low phosphatidylserine exposure, and active ATP-dependent flippases, whereas GPIbα⁻ platelets show signs of stress and GPIbα shedding. Turbulent flow drives late-stage actin depolymerization, promoting even mitochondrial distribution in maturing cells and efficient mitochondrial inheritance to platelets. 

Divergence between transcriptomes and chromatin accessibility during differentiation from a bipotential progenitor cell population to erythroblasts and megakaryocytes

https://www.biorxiv.org/content/10.1101/2025.06.30.662383v1

Using polyA+ RNA deep sequencing of polyA+, the authors characterised the differentiation of the murine megakaryocyte-erythroid progenitor (MEP) into erythroblasts (ERY) and megakaryocytes (MEG). MEPs already express many MEG genes while retaining myeloid programs, whereas ERY induces extensive erythroid-specific genes and represses pan-hematopoietic and MEG genes.Transcription factor occupancy differs between lineages, with MEG genes bound early in progenitors and ERY genes mainly after commitment.

Synergistic effects of deleting the tyrosine phosphatases Shp1 and Shp2 on megakaryopoiesis and thrombopoiesis in mice

https://www.biorxiv.org/content/10.1101/2025.10.24.684367v1

From the authors: Deletion of Shp1 and Shp2 in the MK/platelet lineage in mice results in macrothrombocytopenia and minor effects on platelet function. Defects can be partially explained by reduced Mpl signaling and aberrant megakaryopoiesis in the absence of Shp2 activity.

 

Paradoxic enhancement of mitochondrial capacity in aging-specific megakaryopoiesis from hematopoietic stem cells
https://www.biorxiv.org/content/10.1101/2025.11.10.687744v1

From the authors: Aging-specific MkPs have elevated mitochondrial capacity, the inverse of aged HSCs. Mitochondrial enhancement differentially alters platelet counts in young and old mice. Enhancement of mitochondrial capacity increases platelet repopulation by both young and old HSCs.

Erythropoiesis

Stag2 dependent chromatin remodeling enforces the erythroid-specific Gata1 cistrome

https://www.biorxiv.org/content/10.1101/2025.09.15.676332v1?rss=1

The authors here report that the loss of the cohesin subunit Stag2 alters hematopoietic lineage output by reshaping chromatin accessibility and transcription factor function. In Stag2-deficient mice, erythroid progenitors (EryPs) are reduced and show impaired maturation. RNA- and ATAC-sequencing revealed that GATA1 occupancy shifts from erythroid to megakaryocyte target genes, driving diminished erythroid and enhanced megakaryocyte differentiation, a phenotype recapitulated in human cell models and MDS patient samples.

N6-methyladenosine regulation of mRNA translation is essential for early human erythropoiesis

https://www.biorxiv.org/content/10.1101/2025.11.10.687731v1

This work shows that m6A RNA modification plays stage-specific roles during human erythropoiesis. Using in vitro differentiation of hHSPCs, two critical windows of m6A-methyltransferase (MTase) requirement were identified: in BFU-E, where m6A promotes proliferation, and during the CFU-E to proerythroblast transition, where both m6A-MTase and YTHDF readers are essential for differentiation.

Aspartate transaminases are required for blood development

https://www.biorxiv.org/content/10.1101/2025.09.16.675844v1

Elevated erythropoiesis across multiple models consistently revealed increased aspartate levels, implicating aspartate metabolism in red blood cell production. Genetic deletion of the aspartate aminotransferases GOT1 or GOT2—globally or specifically in erythroid cells—caused anemia marked by early progenitor accumulation, with GOT2 loss producing the most severe phenotype. Despite similar defects, GOT1 and GOT2 loss altered aspartate differently, and neither malate–aspartate shuttle disruption nor NADH redox rescue corrected the anemia. Transcriptomic and epigenetic profiling instead identified dysregulated histone modifications, positioning GOT1 and GOT2 as metabolic–epigenetic regulators essential for erythropoiesis and potential therapeutic targets for anemia.

Blood originates in hypoblasts during embryonic development
https://www.biorxiv.org/content/10.1101/2025.11.07.687183v1

From the authors: Barcode-traced hypoblast fate in human embryo models. The first blood comes from the hypoblast that contributes to hemoglobin+ phagocyte-like cells. CDX2 marks hypoblast blood that sustains oxygen supply in embryos before heart formation. Erythro-core regulatory network endows erythropoiesis to human hypoblasts and phagocytes.

Mammalian PABPC4 is non-essential, but has roles in growth, post-natal survival and haematopoiesis

https://www.biorxiv.org/content/10.1101/2025.11.22.689676v1?rss=1

In this study, the authors investigated the in vivo functions of the cytoplasmic poly(A)-binding protein PABPC4 in mammals. They found that, unlike in non-mammalian vertebrates, PABPC4 is not essential for development, although its loss affected birth weight, post-natal growth, and survival in a partially sex-specific manner. Surprisingly, PABPC4 deficiency caused microcytic red blood cells without reducing hemoglobin levels, and this effect was not intrinsic to red blood cells. These findings provide the first in vivo insights into mammalian PABPC4 function and highlight the limitations of extrapolating from cell-based or non-mammalian studies.

 

Blog post contributed by Alessandro Donada, PhD (Bluesky: @alessandrodonada.bsky.social) of the ISEH Publications Committee. 

Please note that the statements made by Simply Blood authors are their own views and not necessarily the views of ISEH. ISEH disclaims any or all liability arising from any author's statements or materials.