Wild‐type EGFR is activated through binding to extracellular ligands.[23] To investigate whether DDAH1 enhances EGFR dimerization and activates the EGFR‐JAK2‐STAT3 pathway through extracellular ligands, we treated DDAH1‐overexpressing NPC cells with nimotuzumab to block the binding of extracellular ligands to EGFR. The gene discussed is STAT3; the disease is nasopharyngeal carcinoma.