Our observations from Adipoqcre-driven IFNAR deletion are in partial agreement with total body IFNAR−/− and nonhematopoietic IFNAR−/− mice (uncoupling of body weight from severity of glucose dysmetabolism) and FABP4cre-driven IFNAR deletion20 (minimal impact on hepatocellular disease), suggesting a high level of complexity surrounding the contribution of type I IFN/IFNAR axis in obesity. This evidence concerns the gene IFNAR1 and obesity disorder.