Transgenic mice that express PML::RARA in early myeloid cells develop APL with long latency (7, , , –11), suggesting that PML::RARA requires secondary mutations for progression; indeed, several cooperating mutations have been identified in APL (e.g., FLT3, SPI1, GATA2, WT1, KDM6A, and RAS, among others) (12, , , , –17). This evidence concerns the gene KDM6A and acute promyelocytic leukemia.