While the discussions surrounding the prognostic and metabolic implications of hepatic steatosis in ALS remain open, abnormal insulin-like growth factor-1 (IGF-1) axis function alongside lipid redistribution in SOD1G93A mice [88], and dysregulation of lipid metabolism in response to genetic ablation of TDP-43 in mice [73] provide a foundation upon which the beneficial effects of altered hepatic lipid metabolism in ALS can be explored. The gene discussed is IGF1; the disease is fatty liver disease.