A large survey of tumor cell lines expressing wild-type and mutant p53 showed that stabilization of endogenous mutant protein is due to a complete lack of ubiquitination.31 Inhibition of HSP90, either via knockdown or by specific drugs, alleviates the formation of such complexes, leading to reactivation of both MDM2 and CHIP, and mutant p53 degradation. This evidence concerns the gene TP53 and neoplasm.