O‐GlcNAc is implicated in various diseases including cancer, neurodegeneration, cardiovascular disease, and obesity.2 Notably, O‐GlcNAc levels respond to nutrient availability both within cells and in vivo in animal models.1b Transgenic mice overexpressing OGT in fat or muscle tissue exhibit elevated serum leptin and insulin levels in addition to insulin resistance.3 Furthermore, deletion of the gene encoding OGT from neurons of the paraventricular nucleus (PVN) within the hypothalamus of mice results in uncontrolled eating.2b This evidence concerns the gene OGT and obesity due to melanocortin 4 receptor deficiency.