Next, we sought to further investigate the different dependencies conferred by mutant RIT1 and KRAS. RIT1-mutant cells were dependent on several known positive regulators of RAS signaling, including SOS1 and SHOC2 (Fig. 4a), while loss of negative regulators of RAS and genes commonly mutated in Noonan syndrome, such as NF1, SPRED1, and LZTR1, promoted RIT1-induced cell proliferation in erlotinib (Fig. 4a). The gene discussed is SOS1; the disease is Noonan syndrome.