CD4 and autoimmune disease: NLRC3 deficiency in mice increases oxidative phosphorylation and glycolytic capacity, driving Th1 and Th17 cell differentiation, proliferation and IFN‐γ, IL‐2, TNF and IL‐17 production, thus leading to unrestrained generation of activated CD4+ T cells with maximal glycolytic and mitochondrial metabolism [48], which could lead to autoimmune disease progression.