In mice, expression of a KRAS(V14I), SOS1(E846K), or RIT1(A57G) mutation produces many Noonan syndrome-related phenotypes, like growth delay, craniofacial abnormalities, and cardiac defects (Chen et al., 2010; Hernandez-Porras et al., 2014; Takahara et al., 2019). This evidence concerns the gene SOS1 and Noonan syndrome.