Dysregulation of receptor tyrosine kinases (RTKs), including hepatocyte growth factor receptor (HGFR/c-MET) and epidermal growth factor receptor (EGFR), has been implicated in cancer development and progression through a wide range of signaling pathways such as phosphatidylinositol 3-kinase (PI3K)-AKT and mitogen-activated protein kinase (MAPK) [1, 2]. This evidence concerns the gene EGFR and cancer.