It has been shown that glucagon-mediated hepatic ureagenesis is impaired in people with hepatic steatosis that fosters a hyperglucagonemic response to normalize amino acid concentrations.26 Such hyperglucagonemia may drive an increase in hepatic glucose production primarily through GLY rather than GNG.41 In our analysis, there was a strong positive association between liver fat content and the glucagon–alanine index suggesting an impairment in glucagon signaling at the level of hepatic amino acid metabolism. The gene discussed is GCG; the disease is fatty liver disease.