A systemic pro-inflammatory state induced by HFpEF results in coronary microvascular endothelial inflammation, causing reduced nitric oxide (NO) bioavailability and decreasing cyclic guanosine monophosphate (cGMP) content and protein kinase G (PKG) activity, leading to endothelial dysfunction (Paulus and Tschope, 2013). The gene discussed is PRKG1; the disease is inflammation.