PPARα agonists are postulated to also activate gluconeogenesis and affect amino acid metabolism [36], but in this context of sepsis‐induced critical illness, (hepatic) gluconeogenesis was unable to maintain glucose homeostasis as reflected by the lower glycemia and depletion of myofibre glycolytic intermediates, as well as the enrichment of gluconeogenesis pathways in the two pure LCT groups. The gene discussed is PPARA; the disease is Sepsis.