By exploiting a congenic pair of induced pluripotent stem cell (iPSC) lines derived from a familial platelet disorder (FPD) patient, 1 harboring a monoallelic mutation in RUNX1 and the other a corrected allele, in this issue of Blood , Li et al have discovered that negative regulation of NOTCH4 by RUNX1 is required for normal human megakaryocyte (MK) development. Furthermore, the authors demonstrate that suppressing NOTCH signaling, by either genetic or chemical perturbation, significantly enhances MK yield. 1

中文翻译：

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击败巨核细胞

通过利用源自家族性血小板疾病 (FPD) 患者的一对同系诱导多能干细胞 (iPSC) 系，其中 1 个在 RUNX1 中含有单等位基因突变，另一个为校正等位基因，在本期 Blood 中，Li 等人发现RUNX1 对 NOTCH4 的负调节是正常人巨核细胞 (MK) 发育所必需的。此外，作者证明通过遗传或化学扰动抑制 NOTCH 信号显着提高了 MK 产量。1