Leptin has been recently shown to be a crucial factor for the maintenance of the metabolic effects of activated T cells (13) and fasting-induced hypoleptinemia decreased IFN-γ and IL-17 production and the expression of a key glycolytic enzyme in Th17 cells during experimental autoimmune encephalomyelitis (14). The gene discussed is LEP; the disease is experimental autoimmune encephalomyelitis.