Based on preclinical findings showing that reactivation of MAPK signaling through feedback activation of epidermal growth factor receptor (EGFR) was an escape mechanism responsible for intrinsic resistance to a BRAF inhibitor alone [154], a combination therapy of the BRAF inhibitor encorafenib and the EGFR inhibitor cetuximab resulted in significantly improved survival in CRC patients with BRAF V600E mutation [155]. This evidence concerns the gene BRAF and colorectal carcinoma.