Although several small molecular inhibitors targeted on BRAF and MEK such as Dabrafenib and Vemurafenib have passed clinical validation in treatment of BRAF-mutant melanomas [8,9], several studies have demonstrated that drug resistance occurred, and ERK 1/2 can be re-activated after the prolonged administration of inhibitors of receptor tyrosine kinases (RTK), RAF, and MEK [10,11,12]. This evidence concerns the gene MAP2K7 and melanoma.