found that in NSCLC, wild-type P53-induced miR-34 directly binds to the 3′-UTR of PD-L1 to inhibit PD-L1 mRNA expression, representing a potential therapeutic strategy by modulating the tumor immune escape mechanism via the p53/miR-34/PD-L1 axis (43). The gene discussed is TP53; the disease is neoplasm.