KCNJ2 and metabolic syndrome: Arteries from the mice containing the Kir2.1-L222I mutation exhibited dilations to flow comparable to non-dyslipidemic, WT mice independent of the presence of dyslipidemia indicating that rendering Kir2.1 insensitive to cholesterol-mediated suppression was sufficient to restore endothelial function without removing the cholesterol surplus [16••].