We detected the protein expression in murine hearts and found that phosphorylation of STAT3 was remarkably increased at both 4 weeks (p < 0.001) and 8 weeks (p < 0.001) after TAC, and raloxifene decreased the p-STAT3 level significantly at both time points (p < 0.01), which indicated the IL-6/STAT3 signaling was activated in TAC murine hearts (Figures 5(a), 5(b), 5(d), and 5(e)). The gene discussed is STAT3; the disease is persistent truncus arteriosus.