In naturally occurring myxomatous mitral valve disease, accompanied or not by valve regurgitation and prolapse, quiescent VICs are transformed to activated VICs, which exhibit increased cell proliferation and enhanced expression of myofibroblastic protein markers, such as alpha-smooth muscle actin (α-SMA), matrix metalloproteinase 1 (MMP1), and transforming growth factor beta 1 (TGFβ1) (3, 5, 6). The gene discussed is TGFB1; the disease is mitral valve disorder.