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The primary theoretical concern is that sustained NAD+ elevation through chronic NNMT inhibition could activate pathways (PARP, SIRT1) that have context-dependent roles in cancer biology NAD+ supports DNA repair and cellular longevity, but also fuels rapidly dividing cells

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Additionally, the study reported that both extracellular SOD protein and enzyme activity, as well as the levels of reduced TRX1, were markedly decreased in PCa tissues compared to normal tissues [18]

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper

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