Mechanistically, the pharmacological activation of p53, achievable with MDM2 inhibitors, has been shown to induce ligands such as ULBP1 and ULBP2 on cancer cells, promoting NKG2D-dependent cytotoxicity by lymphocytes and providing a clear rationale for combining these inhibitors with NKG2D-redirected CAR-T products [35]. The gene discussed is TP53; the disease is cancer.