CPT1C and neoplasm: In contrast, under some circumstances, AMPK activation by nutrient deficit and metabolic stress may promote tumour survival, by enhancing NAPDH levels via suppression of fatty acid synthesis and enhancement of fatty acid oxidation [120], the latter which may result from AMPK-dependent upregulation of CPT1C [81], and by activating the p38-PGC1 transcriptional axis [121].