In many tumors (e.g., colorectal carcinomas, malignant melanomas, thyroid carcinomas, NSCLC, and others), BRAF is in the permanent “on” state due to an activating V600E mutation in the BRAF gene and relays the growth-promoting signals independently of EGFR pathway activation—the signaling cascade is uncoupled from EGFR by mutant BRAF. This evidence concerns the gene BRAF and non-small cell lung carcinoma.