We conclude that apoptosis occurring in factor-dependent AML blasts following growth factor deprivation is mediated by wild-type p53 (PAb1620+), and that conformational change of p53 to the PAb240+ conformation occurring either by mutation or by the action of autocrine growth factors would permit leukaemic cell survival by suppressing apoptosis. This evidence concerns the gene TP53 and acute myeloid leukemia.