For instance, inhibition of mTOR with the rapamycin derivative everolimus increases cisplatin sensitivity of cancer cells upon p53 pathway restoration [24], implying that a combination of mTOR inhibition and reactivation of wild-type functions in mutant p53 proteins might provide an additional strategy for increasing the sensitivity of cancer cells to standard forms of therapy, such as cisplatin. This evidence concerns the gene TP53 and cancer.