Both showed local amplification of EGFR on 7p and abnormalities in the TP53 region on 17p, confirming the existence of dual driver mutation genotypes; and functionally, the C1_EGFR+ tumor cells that promote proliferation and invasion dynamically transformed into the C2_STAT1+ tumor cells with a highly immunosuppressive and multidrug-resistant phenotype. The gene discussed is EGFR; the disease is neoplasm.