Supported by recent studies showing that the acquisition of aneuploidy drives mutp53-associated GOF phenotypes34, that STING activity is often increased in TP53–mutant compared with wt TP53 tumors77, and that cGAS and STING are required for CIN-driven tumor progression65, our findings provide significant insight into not only the GOF mechanisms of TP53 mutations but also all inactivating mutations of p53 that lead to genomic instability to promote immune suppression and metastasis during tumor development and tumor progression. This evidence concerns the gene TP53 and neoplasm.