TP53 and cancer: Since protein–protein interactions with Bcl‐2 family members that account for non‐transcriptional apoptosis by p53WT (Mihara et al, 2003; Chipuk et al, 2004; Leu et al, 2004; Le Pen et al, 2016) are disrupted by many cancer‐derived p53 mutations, such mutations are believed to be “dual hits” which simultaneously inactivate both DNA binding‐dependent and non‐transcriptional mechanisms of p53‐triggered apoptosis (Mihara et al, 2003; Tomita et al, 2006).