CD8A and lung adenocarcinoma: EGFR inhibition using both TKIs and ligand‐blocking antibody (cetuximab) can also augment MHC‐I and MHC‐II expression, potentially via its effect on the interferons (IFN)‐γ receptor complex, class II major histocompatibility complex transactivator (CIITA) mRNA, and/or direct effect on the promoter of MHC genes.[211] But it was also reported that in EGFRmut lung adenocarcinoma, MHC‐I genes were downregulated to evade CD8+ T cells, and the level of MHC class II molecules was enhanced to engage with CD4+ Tregs[212] and confer suppressive functions to Tregs.[213]