They include (1) agents inhibiting cell signaling pathways (such as EGFR and PI3K/mTOR), resulting in the downregulation of ΔNp63; (2) conventional chemotherapy with cisplatin and other genotoxic agents, which induce activation of Tap63 and disruption of ΔNp63, furthermore, ΔNp63 levels have been reported to confer cisplatin sensitivity to subsets of squamous cell carcinomas and breast cancers [42,43]; and (3) the use of targeted ultraviolet light, to degrade P63 in anatomically accessible urothelial cancers. The gene discussed is EGFR; the disease is breast carcinoma.