CD274 and Thyroid adenoma: Several compounds such as Metformin and BMS1166 disrupted the N‐glycosylation modification of PD‐L1 and thereby prevented its ER export and triggered endoplasmic reticulum‐associated degradation.[19, 20] Depletion of THADA (thyroid adenoma associated gene), which is involved in PD‐L1 ER to Golgi trafficking, induced ER retention and degradation of PD‐L1.[21] Therefore, exploring the regulatory mechanism and critical regulators of PD‐L1 intracellular distribution would be beneficial for the development of targeted PD‐L1 small molecule inhibitors.