Accumulating evidence implicates the amyloid-like aggregation of mutant p53 in not only the protein’s loss of tumor suppressor function, but also its oncogenic gain of function (i.e., acquisition of activities that promote tumorigenesis, metastasis, and chemoresistance), as well as the prion-like propagation of these phenotypes (in other words, the spread of mutant p53 aggregates to neighboring healthy cells to seed aggregation of endogenous WT p53) [164,206,207,209,214,218,219]. This evidence concerns the gene TP53 and neoplasm.