Whereas, Cole et al. reported that absent or unfunctional DNMT3A protects Ctsg-PML/RARA mice against APL (58), Mayle et al. and Yang et al. argued that after a long period of latency, DNMT3A deficient mice are prone to developing both myeloid and lymphoid malignancies (59, 60). This evidence concerns the gene PML and acute promyelocytic leukemia.