Several mechanisms may underlie the stabilization of mutant p53 in cancer cells, including: the presence of tumor-specific stress signals that might normally function to stabilize WT p53, the inability of most mutant p53 proteins to induce the transcription of MDM2, and the ability of mutant p53 proteins to complex with members of the heat shock protein family, induced by the unfolded protein response often active in tumors, which stabilize mutant p53 proteins by preventing interaction with MDM2 (Wawrzynow et al. 2018; Mantovani et al. 2019). This evidence concerns the gene MDM2 and neoplasm.