Increased EGFR signaling through autocrine activation caused by BRAF-independent c-Jun signaling or loss of full-length BRAF (V600E) consistent with the expression of a truncated form of the mutant protein has been the mechanisms of acquired resistance in NSCLC cell lines that were sequentially treated with vemurafenib for BRAF(V600E) mutations [139]. The gene discussed is BRAF; the disease is non-small cell lung carcinoma.