Although evidence regarding the association between reductions in intestinal muscularis propria thickness and nutritional status is limited, studies using the experimental autoimmune encephalomyelitis (EAE) model have demonstrated increased proinflammatory Th1/Th17 cytokine expression and reduced regulatory T-cell populations in the gut lamina propria, Peyer’s patches, and mesenteric lymph nodes, accompanied by a decrease in duodenal muscle thickness (71). The gene discussed is NELFCD; the disease is experimental autoimmune encephalomyelitis.