STK10 emerges from the platelet kinome shadow

fetal resistance to MLL::ENL-driven leukemogenesis, the implications of this work extend beyond the immediate findings, opening several avenues for future investigation.Notably, transcriptional changes occur without major shifts in chromatin accessibility, raising the possibility that MLL::ENL may bind different genomic targets depending on developmental stage.Investigating whether the fusion protein engages distinct cofactors or binding sites in fetal vs postnatal progenitors would be crucial.One important question is whether similar fetal resistance mechanisms can be observed in human hematopoietic progenitors, such as those derived from fetal liver or cord blood.Recent studies using the MLL::AF4 fusion in primary human fetal liver CD34 + cells show that infant acute lymphoblastic leukemia (ALL), but not childhood ALL, maintains fetal-specific gene expression programs, supporting the role of developmental context in human cells leukemogenesis.9