BRAF and cancer: Several studies [25, 41, 44] have reported that dual inhibition of MAPK and autophagy caused by a MAPKi can specifically improve clinical efficacy in BRAFV600E tumors; however, excessive autophagy can also cause cancer cells to undergo “autophagic cell death” or “type II programmed cell death” [42], and our research proved this point and provided another solution to vemurafenib resistance: BRAF inhibition and autophagy activation promoted by a MAPKi had a lethal effect on tumors.