In this study, we examined whether a novel anti-EGFR mAb EMab-17 is useful for the treatment of mCRC with KRAS p.G13D mutation via ADCC and CDC activities, rather than via neutralization of the EGFR signaling to promote EGF-dependent cell proliferation, as CRC cells with KRAS mutations bypass the EGFR pathway. This evidence concerns the gene EGFR and colorectal carcinoma.