It has been suggested that tumor cells acquire resistance to EGFR inhibitors or antibodies through the following three different mechanisms—(1) EGFR mutations T790M or S492R; (2) activation of a bypass signaling pathway, such as HER2 upregulation or KRAS activation; and (3) impairment of a pathway that is essential for EGFR tyrosine kinase inhibitor-mediated apoptosis [34]. Here, ERBB2 is linked to neoplasm.