To date, preclinical and clinical studies have shown that EGFR-TKIs can induce antitumor immunity through the following [45, 79, 102, 107, 108, 153–156]: potentiating induction of class I (MHCI) and II (MHCII) molecules; promoting Foxp3 degradation to attenuate the inhibitory function of Tregs; reducing the infiltration of Tregs in the TME and inhibiting tumor growth; and enhancing the cytotoxicity of cytotoxic T lymphocytes (CTLs) that mediate antitumor immune response, reduce T cell apoptosis, and increase IFN-γ secretion to enhance the immune system response. This evidence concerns the gene IFNG and neoplasm.