When PML-RARA is expressed in mice using regulatory elements from the human or mouse cathepsin G gene (CTSG/Ctsg) or the human S100A8 (MRP8) promoter/enhancer, it can initiate APL; when RARA or PML-RARA are expressed in mouse bone marrow cells via retroviral transduction, both can decrease myeloid maturation and increase self-renewal [1], [2], [3], [4]. This evidence concerns the gene PML and acute promyelocytic leukemia.