Next, based on the role of VAT in increasing levels of circulating FAs in obesity [12–14], we predicted that inhibiting lipolysis in VAT from obese mice and humans ex vivo would restore endothelial Kir2.1 function and prevent the VAT-mediated increase in FA uptake, again replicating effects that were previously observed when endothelial CD36 was downregulated. The gene discussed is KCNJ2; the disease is obesity disorder.