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Intracellular excess copper can activate transcription factor EB (TFEB), upregulate the expression of autophagy protein 5 (ATG5), sequestosome 1 (SQSTM1), and microtubule-associated light protein 3 (MAP1LC3) 1, and regulate the AMP-activated protein kinase–mechanistic target-of-rapamycin (AMPK-mTOR) pathway to induce autophagy [70]

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Consequently, it can be hypothesised that the administration of NAD + -boosting drugs may result in the regulation of ChREBP by means of pathways other than those involving the NAD +/Sirtuin pathways