Regulatory T cells (Tregs) normally maintain balance in the immune system, but Treg dysfunction can lead to inflammation and immune disorders. The protein PPARγ enhances Treg generation and function, so it’s a promising therapeutic target for these conditions. However, the mechanisms of PPARγ’s effects on Tregs are unclear. To learn more, researchers recently tested the effects of several PPARγ-activating drugs on Tregs derived from mouse lymph node cells. The activators increased Treg production and the expression of immunosuppressive molecules important for Treg function. They also enhanced Tregs’ energy supply by upregulating CD36 and CPT1, two proteins involved in fatty acid oxidation (FAO). Furthermore, PPARγ activation increased N-linked glycosylation, a process that links carbohydrate molecules to proteins and thereby altered the cell-surface abundance of the receptors TβRII and IL-2Rα, affecting the TGF-β/Smad and IL-2/STAT5 signaling pathways. Inhibition of the enzyme PFK was key to the effects of PPARγ activation on FAO and N-linked glycosylation. Although more work is needed, the findings help clarify the connection between PPARγ and Tregs and provide numerous potential targets for immune system regulation.