The mechanisms underlying the tumor selectivity may include altered signaling pathways of ataxia telangiectasia mutated (ATM), epidermal growth factor receptor (EGFR), p53, PKR, Ras, RB/E2F/p16, Wnt, anti-apoptosis, or defects in cellular innate immune signaling pathways or hypoxia conditions in the TME (1, 3, 19, 20). This evidence concerns the gene EGFR and neoplasm.