This response is a manifestation of innate resistance.8,9 Recent studies reveal that EGFR kinase-independent activity also promotes cancer cell survival and chemoresistance.10–12 Hence, targeting EGFR by inducing degradation rather than inhibition of kinase activity could be a more effective and complete approach to repress EGFR in NSCLC treatment. The gene discussed is EGFR; the disease is cancer.