The ability of NK cells to lyse tumor targets independent of EGFR, RAS and BRAF status combined with the observation that cetuximab can enhance this cytotoxic effect in EGFR expressing tumors regardless of RAS and BRAF mutational status is an added advantage as it can result in effective target cell lysis of tumors responsive or non-responsive to cetuximab monotherapy. This evidence concerns the gene BRAF and neoplasm.