112 Targeting the PGC1α/CEBPB/CPT1A/FAO signaling axis by etomoxir (ETO) or genetic knockdown could be a potential strategy to improve the therapeutic effects of radiotherapy in NPC.113 Mechanistic studies of abnormal tumor fatty acid metabolism and radiotherapy resistance will help enrich our understanding of tumor lipid metabolism reprogramming and provide new perspectives and novel molecular targets for tumor radiotherapy resistance. The gene discussed is CPT1A; the disease is neoplasm.