MK-1775 significantly elevated the efficacy of cisplatin, vorinostat (HADC inhibitor), or alisertib (aurora kinase A inhibitor) in HNSCC cells expressing high-risk mutp53 both in vitro and in vivo, while tumor cells bearing wildtype p53 displayed minimal response to MK-1775 (114–117). This evidence concerns the gene TP53 and neoplasm.