Lower p16INK4aexpression in AML samples of patients of older age predicts for reduced OS.Further studies unraveling the regulation and molecular mechanisms responsiblefor the down-regulation of p16INK4a during aging in AML are awaited.Striking in this perspective is our observation that BMI1, a potent repressorof p16INK4a, was significantlyinversely correlated with p16INK4a in older (P = <.001, rho = -.274, n = 175) and not inyounger (P = .322, rho = -.075, n = 175) AML patients. This evidence concerns the gene BMI1 and acute myeloid leukemia.