This study suggests that the p53‐IFI16‐NF‐κB axis under genotoxic stress may be the central hub for tumour cells to achieve dual adaptation of ‘pro‐survival and anti‐apoptosis’, not only recruiting immune cells through inflammatory signals to promote tumour progression, but also maintaining the survival of malignant clones through proliferation signals. This evidence concerns the gene NFKB1 and neoplasm.