Using a molecularly annotated platform of 85 mCRC patient-derived xenografts, Bertotti et al. [97] identified ERBB2 amplification as an actionable liability in cetuximab-resistant CRCs harboring wt KRAS/NRAS/BRAF/PIK3CA. Moreover, they showed that the addition of anti-ERBB2 agents to anti-EGFR monoclonal antibodies overcame resistance and inhibited tumor growth[97]. This evidence concerns the gene NRAS and neoplasm.