The number and function of Tregs can be regulated by related signaling pathways; for example, it has been verified that the IL-21-driven mechanistic target of rapamycin (mTOR) activation blocks the development of Tregs and underlies the dysfunction of Tregs in SLE (15); In addition, type 1 sphingosine-1-phosphate receptor (S1P1) signaling negatively controls the thymic generation and suppressive function of tTregs, depending on the Akt–mTOR axis (16). Here, MTOR is linked to systemic lupus erythematosus.