Angiotensin II (Ang II), which played an significant role in the excessive sympathetic excitation and development of HF, was an important component of the renin–angiotensin–aldosterone system (RAAS) system; its dependence on ANS activation played an vital role in the adverse hemodynamic and LV remodeling responses to myocardial infarction, possibly via oxidative stress (Taylor-Piliae, 2003; Ren et al., 2016). The gene discussed is REN; the disease is hydrops fetalis.