More specifically, the MAP kinase cascade is frequently hyperactivated in lung and other cancers owing to the overexpression or mutation of receptor tyrosine kinases, such as EGFR, anaplastic lymphoma kinase (ALK), MET proto-oncogene (MET), and other downstream effectors, which are most commonly rat sarcoma virus gene (RAS) and proto-oncogene B-Raf (BRAF). This evidence concerns the gene EGFR and cancer.