We verified this hypothesis by comparing murine and human AML cell lines with high or low expressions of p16INK4A and/or p18INK4C and murine Cdkn2a−/− vs. Cdkn2a+/+ BCR-ABLp185+ cells modelling acute lymphoblastic leukaemia (ALL). The gene discussed is CDKN2A; the disease is acute myeloid leukemia.