One of these studies found that there was lower mitochondrial membrane potential, lower proton leak (oligomycin, ATP synthase inhibitor, resulting in the depletion of proton motive force), lower ATP production in CD8+ T cells from ME/CFS/SEID patients compared with HC participants, also lower glycolysis at rest in both CD8+ and CD4+ cells from ME/CFS/SEID patients [12, 27]. This evidence concerns the gene CD8A and myalgic encephalomeyelitis/chronic fatigue syndrome.