Overexpression of DDAH1 in NPC cell lines increases cisplatin resistance both in vitro and in vivo through binding to the intracellular domain of epidermal growth factor receptor (EGFR), enhancing its dimerization and phosphorylation, thereby promoting the activation of the JAK2‐STAT3 pathway, which is dependent on EGFR and extracellular ligands and can be weakened by nimotuzumab. This evidence concerns the gene DDAH1 and nasopharyngeal carcinoma.