Unlike many solid tumours, in which one of the most common events leading to a block in apoptosis is a genomic loss of p53 by either deletion or mutation, the TP53 locus is wild-type in most cases of non-complex karyotype de novo AML (Haferlach et al, 2008; Rücker et al, 2012; Cancer Genome Atlas Research Network, 2013), suggesting that alternate mechanisms are at play to block apoptosis in the majority of AML cases. The gene discussed is TP53; the disease is acute myeloid leukemia.