However, BRAF mutation alone is not sufficient for malignant transformation [65] as demonstrated by recent studies that point out the pivotal role of WNT signaling hyperactivation in the “serrated pathway” [66] and suggest how mutant BRAF, phosphorylating the transcriptional co-repressor MAFG, via the BRAF-MEK-ERK axis, induces CpG-islands hypermethylation [5, 67]; this could be the molecular confirmation of the link between BRAF mutation and CIMP-H/MSI status in CRC [68]. Here, BRAF is linked to colorectal carcinoma.