Torasemide has a strong diuretic effect and an anti-fibrotic effect for which a mechanism has been recently proposed: torasemide inhibits procollagen type I carboxy-terminal proteinase activation as well as lysyl oxidase expression and collagen cross-linking in patients with heart failure [11], [12], resulting in normalization of left ventricular stiffness. The gene discussed is COL1A2; the disease is heart failure.