With approximately comparable citations in their respective studies, Petersen et al. [27] found that insulin resistance redirects postprandial energy from muscle glycogen synthesis to hepatic lipogenesis, explaining dyslipidemia independent of TNF-α/IL-6, while Lin et al. [28] showed that FGF21 requires adiponectin to mediate systemic metabolic effects, as adiponectin knockout mice resisted FGF21’s improvements in glucose tolerance and hepatic steatosis. This evidence concerns the gene FGF21 and fatty liver disease.