The question was addressed here by examining 1) the expression of AdipoR1 in microvessels from patients with and without CAD, 2) the role of AdipoR1 in adiponectin-induced restoration of NO as the primary mediator of FID in diseased arterioles, and 3) whether osmotin, a plant-derived stress protein whose receptor shares homology with AdipoR1, can serve in the same capacity and promote vasodilation that relies on the formation of NO. The gene discussed is ADIPOQ; the disease is coronary artery disorder.