Etoposide suppresses STT3 activity through EMT inhibiting, thus hindering cPD‐L1 glycosylation and promoting its degradation, ultimately inducing tumor‐specific immunity.[99, 114] EGFR inhibitor gefitinib restrains B3GNT3 activity, leading to decreased cPD‐L1 glycosylation and increased degradation, which in turn provides a new insight to increase the efficacy of immunotherapy in lung adenocarcinoma patients.[98] SAFit is shown to facilitate PD‐L1 degradation by inhibiting FKBP51s‐mediated glycosylation in glioma.[101]. The gene discussed is B3GNT3; the disease is neoplasm.