Since a residual p-ERK2 pathway is necessary to induce ATF4-dependent cell death [37], and disruption of SHOC2 would only affect oncogenic KRAS signaling, the blockade of CRAF activation by disrupting the SHOC2 complex might be a therapeutic route to induce apoptosis in tumor cells but with less toxicity for the patient. The gene discussed is KRAS; the disease is neoplasm.