EGFR is overexpressed in many cancers, and its activation is related to the tumor microenvironment; for example, oxidative stress-mediated activation of EGFR leads to failure of EGFR to undergo entry into early endosomes for subsequent degradation, resulting in prolonged activation of EGFR signaling, tumorigenesis, and malignancy [15, 16]. This evidence concerns the gene EGFR and neoplasm.