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Recently reported, deacetylation based on NAD+ signaling was able to enhance the expression of key proteins implicated in PI3KIII-dependent autophagy or promoted Parkin-independent mitophagy through the liver kinase B1 (LKB1)/AMPK/tuberous sclerosis complex 2 (TSC2) or the SIRT3/FUNDC1 pathways [9]

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On the other hand, the CXXCBAH1 linker undergoes a helix-to-loop conformational transition and is positioned along the catalytic cleft of DNMT1 to inhibit the interaction between DNMT1 and DNA

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