Thus, it is likely that type I IFN/IFNAR modulation of intrahepatic immune cells (e.g. CD8+ T cells) may be the larger governing factor to orchestrating obesity-driven NAFLD pathogenesis, while type I IFN/IFNAR activation of adipocytes underscores the severity of glucose dysmetabolism. This evidence concerns the gene IFNAR1 and obesity due to melanocortin 4 receptor deficiency.