Upon nutrient depletion, SIRT1 deacetylates nuclear LC3 at lysine residues K49 and K51, which leads to the interaction between LC3 and the nuclear protein DOR (diabetes- and obesity-regulated nuclear factor), which is required for the translocation of both LC3 and DOR to the cytoplasm. This evidence concerns the gene MAP1LC3A and obesity due to melanocortin 4 receptor deficiency.