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We surmise that, on the one hand, KIRC cells may obtain more acetyl-CoA for lipid synthesis because NNMT upregulation can restrain polyamine catabolism by downregulating SAM levels, where MAT1A (S-adenosylmethionine synthase isoform type-1) and MAT2A ( S -adenosylmethionine synthase isoform type-2) expression levels are similar to normal kidney cells [57]

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