Cancer cells exhibit the ability to inhibit PD-L1 degradation and maintain its protein stability by deubiquitination or glycosylation of PD-L113,22,23, while PD-L1 induces proteasome-dependent degradation by the GSK3β pathway in response to osimertinib or MTI-31 in EGFR mutant non-small cell lung cancer (NSCLC) cells33,34, and MTI-31 induces PD-L1 degradation and increases T-cell proliferation, which is associated with inhibition of tumor growth in a lung cancer tumor model34. The gene discussed is EGFR; the disease is neoplasm.