Analysis of human and canine valve specimens has also demonstrated increased activation of TGF-β/Smad signaling in both syndromic and non-syndromic myxomatous valves and mitral valve prolapse, suggesting that TGF-β/Smad signaling may play a causal role in non-syndromic MVD (10–14). The gene discussed is TGFB1; the disease is mitral valve disorder.