In addition, a naturally-occurring human Shoc2 mutant was described that yields high phospho-ERK levels, causing a Noonan-like syndrome [15]; this gain-of-function mutation in Shoc2 (S2G) generates an aberrant N-myristoylation site, resulting in a Shoc2 protein constitutively plasma membrane targeted [15] and unable to translocate to late endosomes [35]. This evidence concerns the gene SHOC2 and Noonan syndrome.