A TAC operation leads to cardiac hypertrophy through ventricular wall pressure overload, while AngII promotes cardiac hypertrophy through vasoconstriction, activation of the RAS, water and sodium retention, and cardiotoxicity, all of which ultimately activate the STAT3 and p-38/MAPK signaling pathways (Pan et al., 1997; Brancaccio et al., 2006). The gene discussed is AGT; the disease is persistent truncus arteriosus.