This increase of steroid sulfatase in the liver of transgenic mice has been interpreted as a mechanism to counterbalance metabolic dysfunction, since overexpression alleviated dysmetabolism in high-fat diet and ob/ob models of obesity and type 2 diabetes, resulting in reduced body weight, improved insulin sensitivity, and decreased hepatic steatosis and inflammation. Here, STS is linked to obesity due to melanocortin 4 receptor deficiency.