To begin exploring the mechanism of how BCR-ABL ALL was expanding more rapidly in vitamin D sufficient versus deficient mice in vivo (Figs. 1–2, 4A), we examined the effect of 1,25(OH)2VD3 treatment on BCR-ABL Arf−/− leukemia cells in vitro. This evidence concerns the gene CDKN2A and acute lymphoblastic leukemia.