It has been shown that, e.g., in EGFR-mutant lung cancer, the EGFR signalling pathway is activated, leading likely to an uninflamed tumour microenvironment [74] due to the lowered activity of pro-inflammatory interleukins such as IL-6, IL-8, or TNF-α and due to the increased activity of immunosuppressive factors such as TGF-β, resulting in tumour escape or immunosuppression. This evidence concerns the gene EGFR and neoplasm.