Although numerous studies have identified selected clinical parameters such as age, gender, HF etiology, LVEF, NYHA class, and NT-proBNP level as independent predictors of adverse HF prognosis [1, 2], considerable data suggests that objective measure of subclinical disease and pathophysiological derangements related to HF, such as neurohumoral activation, endothelial dysfunction, or low-grade inflammation, may provide estimation of morbidity and mortality risk beyond clinical parameters [4, 9, 12, 23–25]. The gene discussed is NPPB; the disease is endothelial dysfunction.