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Mitochondrial fatty acid oxidation (FAO) is the primary pathway for the degradation of fatty acids and promotes NADPH and ATP production. Our previous study demonstrated that upregulation of carnitine palmitoyl transferase 1 A (CPT1A), the key regulator of FAO, promotes radiation resistance of nasopharyngeal carcinoma (NPC). In this study, we found that high expression of PGC1\u03b1 is associated with poor overall survival in NPC patients after radiation treatment. Targeting PGC1\u03b1 could sensitize NPC cells to radiotherapy. Mechanically, PGC1\u03b1 binds to CCAAT\/enhancer binding protein \u03b2 (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. Our results revealed that the PGC1\u03b1\/CEBPB\/CPT1A\/FAO signaling axis promotes radiation resistance of NPC. 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