IL-6 promotes glucose uptake and fatty acid oxidation–induced lipolysis and regulates muscle–adipose tissue crosstalk.30 The systemic immune response we observe in ALS may be linked to the state of hypermetabolism and of lipid dysregulation now widely recognized in ALS.31 Hence, the observed late IL-6 regulation may reflect the increasing metabolic imbalance associated with the disease process in ALS. Here, IL6 is linked to amyotrophic lateral sclerosis.