Inactivation of p53 is associated with a dramatic activation of self-complementary transcripts (double-stranded RNAs) from the widespread repetitive DNA elements such as Alu-repeats.35 The double-stranded RNAs elicit a strong type I IFN response that hinders proliferation of cancer cells thereby putting a strong selective pressure and forcing inactivation of the IFN response mechanisms so that further evolution and expansion of cancer cells35 is allowed. This evidence concerns the gene TP53 and cancer.