Unlike the TKIs that can induce EGFR dimerization without activation (219, 220, 228) and are only effective in cancers bearing kinase-activating mutations in EGFR, anti-EGFR mAbs are capable of reducing EGFR proteins by shifting the ligand induced EGFR endocytosis toward the non-recyclable stage, the late-endosomal stage where EGFR is to be degraded rather than being recycled back to the plasma membrane as most of the early-endosome localized EGFR are programed to do (9). Here, EGFR is linked to cancer.