Data from patients with KRAS wild-type mCRC in the GALGB/SWOG 80405 clinical trials revealed that patients with the primary tumor site of mCRC in the left colon could benefit from cetuximab.[34] Her3 activation is responsible for cetuximab resistance developed under the pressure of the EGFR blockade,[35] which may reduce cetuximab efficacy in patients with CRC.[36] Kawakami et al[37] indicated that high Her3 expression is an essential factor in cetuximab resistance and suggested that high expression of Her3 is associated with cetuximab treatment failure. This evidence concerns the gene ERBB3 and neoplasm.