To date, different mechanisms of resistance to anti-EGFR drugs in CRC have been described including reduced antibody-receptor interaction, activation of parallel subsidiary pathways, constitutive activation of EGFR effector molecules, reactivation of pro-angiogenic factors, dysregulation of EGFR internalization and degradation [20,35,36]. The gene discussed is EGFR; the disease is colorectal carcinoma.