Moreover, miR-1 overexpression also inhibited cardiac fibrosis and apoptosis by reducing the mRNA expression of transforming growth factor beta-1 (Tgfb1) and increasing protein expression of Bcl-2, while reducing the level of Bax, thereby altering the Bcl-2/Bax ratio [105]. The gene discussed is TGFB1; the disease is fibrosis.