PD‐L1 expression is regulated by interferon‐γ (IFN‐γ).5 Binding of IFN‐γ to the IFN‐γ receptor activates the JAK/STAT pathway, resulting in enhanced expression of PD‐L1 and β2‐microglobulin (β2‐MG), a component of the major histocompatibility complex (MHC) class I.6 These molecules are important for tumor immunity, they are not only the target molecules of ICIs but are also responsible for resistance to anti‐cancer immunotherapy. The gene discussed is SOAT1; the disease is cancer.