BrafL597V mice expressing an L597V mutation, causative of NS, developed typical features, including short stature and cardiac enlargement as well as an increased cardiomyocyte cross-sectional area, indicative of cardiac hypertrophy, while BrafQ241R, expressing the Braf Q241R mutation, which is the most frequent gain-of-function mutation in CFC syndrome, showed cardiomegaly, expanded cardiac valves, ventricular noncompaction, and VSDs, through activation of the RAS–MAPK pathway, as established by using MEK inhibitors [27]. This evidence concerns the gene MAP2K7 and cardiac hypertrophy.