To our knowledge, RAR rearrangement-mediated variant APL possibly exhibited partially similar mechanisms with typical APL, but the details were truly different for each fusion due to the distinct partner of RAR. Furthermore, the leukemogenesis of some variant APLs even did not rely on the RAR rearrangement, while MLL rearrangement, NPM1 rearrangement, and some specific fusion or gene mutation could generate variant APL partially via down-regulating RAR expression. This evidence concerns the gene KMT2A and acute promyelocytic leukemia.