INS and thanatophoric dysplasia: The pathophysiological mechanisms that have been studied to explain the association of TD and NAFLD are insulin secretion and lower hepatic β-oxidation, which favors the accumulation of triglycerides and lipid mediators such as diacylglycerols, sphingomyelins, and ceramides that induce insulin resistance, impaired suppression of gluconeogenesis, and stimulation of de novo lipogenesis in the liver [35].