In this issue of Blood, Chiu et al report the presence of functional redundancy between the transcription factors lymphoblastic leukemia 1 protein (LYL1) and stem cell leukemia protein (SCL) in the process of megakaryocyte (MK) maturation and platelet production in mice.(1) This discovery may provide an answer to the long-standing mystery of why mutations in SCL protein do not present with any phenotypic platelet disorder, whereas mutations in its binding partner proteins GATA1, FLI1, RUNX1, and GFI1B cause hereditary thrombocytopenia.
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