In an elegant set of experiments with various transgenic mouse models, Andres-Hernando et al. showed that the V1b receptor, but not V1a receptor, was required for the development of fructose-induced metabolic syndrome.11 After treatment with fructose in the diet, the V1b receptor knockout mice had lower body weight as well as triglyceride, alanine aminotransferase, insulin, leptin levels, and liver steatosis compared with wild-type littermate controls. Here, AVPR1B is linked to metabolic syndrome.