Yamaoka et al. (2017) summarized four general mechanisms of anti-EGFR antibody and EGFR tyrosine kinase inhibitor resistance in cancer cells: (i) secondary mutations in the EGFR gene; (ii) resistance to apoptotic cell death; (iii) phenotypic transformation (e.g., tumor cells activating stem cell-like characteristics); and finally, (iv) activation of alternative signaling pathways [33]. The gene discussed is EGFR; the disease is neoplasm.