Available evidence supports the view that inappropriate cell survival from the onset of the oncogenic process, for example via failure of p53 to initiate apoptosis (usually because of mutations that are common in various cancers) to signal apoptosis by transcriptional activation of the pro‐apoptotic BH3‐only BCL2‐family members PUMA and NOXA, is likely to be a key pathway in multistep oncogenesis enabling survival of cells harboring harmful DNA damage.47 Here, BCL2 is linked to cancer.