Glucose metabolism was crucial for the activation, proliferation and differentiation of CD4+ T cells [36], contributing to the patho-immunological response in SLE via the production of overactive T effector cells (including Th1 and Th17 cells) and proinflammatory cytokines (including interferon (IFN)-γ and interleukin (IL)-17). The gene discussed is IFNG; the disease is systemic lupus erythematosus.