In addition, agomir-125b or agomir-NC was tail intravenously injected into TAC mice, and the results indicated that TAC treatment markedly increased BAK1 protein level compared with the sham group (p < 0.001), and miR-125b overexpression observably decreased TAC-induced BAK1 expression compared with the agomir-NC group (p < 0.05) (Fig. 4D). The gene discussed is BAK1; the disease is persistent truncus arteriosus.