Although here it is not sure whether AMPK directly regulates phosphorylation of TET1, our findings suggest the notion that TET1 plays an important role in glucose metabolism through AMPK-dependent signaling by directly interacting with and activating SIRT1, supporting the notion that TET1 loss-of-function led to increased energy expenditure and protection from diet-induced obesity, insulin resistance, and glucose tolerance (Damal Villivalam et al., 2020). This evidence concerns the gene SIRT1 and obesity due to melanocortin 4 receptor deficiency.