Key findings:• In mice, TNFα and IFNγ suppress VAT-Treg accumulation indirectly [21,23], while IFNα derived from pDCs directly reduces survival and proliferation of VAT Tregs through IFNAR1 signaling [9]• In humans, IFNγ reduces VAT-Treg suppressive function by promoting expression of inhibitory molecule PD-1 [24]Questions remaining:• What is the molecular mechanism by which IFNα disrupts VAT Tregs?• Do other obesity-associated inflammatory molecules such as IL-1β and IL-6 disrupt VAT Treg homeostasis and function? The gene discussed is IFNAR1; the disease is obesity disorder.