XIST and transient myeloproliferative syndrome: Since it has been shown in mice that Xist can initiate chromosome silencing specifically in somatic hematopoietic progenitor cells46, it can now be considered that dosage-compensation of chromosome 21 expression in DS-TMD children might eventually be developed as a therapeutic ex vivo or in vivo strategy, or even conceivably in fetal liver in utero47,48 (the origin of cells that give rise to TMD and leukemia).