The rationale for the synergistic anti-tumor activity of cetuximab plus avelumab could be based on a double mechanism, such as the direct inhibition of two biologically relevant targets for NSCLC, EGFR and PD-L1 [6–8] as well as the ability of these two IgG1 mAbs to bind natural killer (NK) cell FC receptors (FCG3A/CD16) and to induce antibody-dependent cell cytotoxicity (ADCC) [9]. The gene discussed is EGFR; the disease is neoplasm.