EGFR and neoplasm: 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.