Liver-specific deficiency of KDM6B leads to intrinsic defects in β-oxidation, resulting in hepatosteatosis, glucose and insulin intolerance, whereas its overexpression selectively inhibits lipid levels without increasing glucose levels in patients with obesity, hepatosteatosis, and type 2 diabetes (Seok et al. 2018). This evidence concerns the gene KDM6B and obesity due to melanocortin 4 receptor deficiency.