Hence, it is conceivable to hypothesize that: (a) in AML, PMF and CML, HERC1 might act as an oncosuppressor [36] and (b) though genotypically different all these myeloid disorders share a common HERC1 transcriptional repressor mechanism that in CML it is positively regulated by BCR-ABL1. Here, HERC1 is linked to acute myeloid leukemia.