Moreover, it is postulated that temporary elevations in sarcolemmal membrane permeability may facilitate the release of H-FABP into the bloodstream.9,10 Even following short-term ventricular stress, this “wounding” of myocytes was found, and it is likely to have substantial impact in different autocrine and paracrine pathways involved in pathogenesis of the heart failure.9 The gene discussed is FABP3; the disease is heart failure.