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. The gene discussed is FGF21; the disease is Insulin resistance.