EGFR and non-small cell lung carcinoma: In terms of possible mechanisms explaining immunosuppressive microenvironment in NSCLC with EGFR ex20ins, we explained that ex20ins could activate the downstream MAPK and PI3K/AKT signaling pathways, resulting in AKT1 recruitment and impairing TANK‐binding kinase 1 (TBK1) phosphorylation, and suppress interferon regulatory factor 3 (IRF3), thus disrupting the stimulator of interferon gene (STING) signaling and suppressed type I and II interferon response and antitumor immune responses (Figure 3C), which had been currently reported by in vitro researches.43, 44