However, functional inactivation of p53 or of its pathway appears to be a requisite for transformation; loss of p53 function in cancer cells with wild-type TP53 is often caused by abnormalities in p53-regulatory proteins, including overexpression of mouse double minute 2 (MDM2)/MDMX, deletion of CDKN2A/ARF, and alterations in ATM. Contrary to solid tumours, the CDKN2A locus and ATM are rarely altered in AML. The gene discussed is ATM; the disease is acute myeloid leukemia.