Several mechanisms of acquired resistance following BRAF/MEK inhibitor treatment have been identified in other types of BRAFV600E mutated tumors, such as melanoma and colorectal cancer involving, for instance, either the reactivation of the MAPK pathway, or activation of parallel signaling cascades such as the PI3K/AKT pathway, or acquired mutations of the RAS gene family [30,31,32]. This evidence concerns the gene AKT1 and colorectal cancer.