It has been proposed that overexpression of the Shoc2 mutant with the S2G substitution (serine 2 is mutated to glycine), found in Noonan-like syndrome patients, results in N-myristoylation and targeting of this Shoc2 mutant to the plasma membrane, and enhances EGFR-dependent ERK1/2 activity [22]. The gene discussed is MAPK3; the disease is Noonan syndrome.