The abovementioned metabolic characteristics of SLE T cells, such as enhanced glycolysis, lipid synthesis, glutaminolysis, and highly activated mTOR, all favored Th17 differentiation and function, which suggest the metabolic abnormalities of SLE T cells is the underlying mechanism of Th17/Treg imbalance in SLE patients (Figure 1). This evidence concerns the gene MTOR and systemic lupus erythematosus.