Studies have shown that transgenic expression of EGFR mutants in mouse lung tissue induces the development of lung adenocarcinoma, and treatment with EGFR-targeted tyrosine kinase inhibitors (TKIs) leads to significant tumor regression [5], indicating that activating mutations in the EGFR tyrosine kinase domain increase EGFR activity and accelerate lung tumorigenesis. This evidence concerns the gene EGFR and neoplasm.