This may be explained by the fibrogenesis stimulus induced by the sST2 in the context of an increased LV filling pressures—patients with HFpEF are generally hypertensive and obese, with elevated Angiotensin II circulating levels, an aspect that is furtherly inducing myocardial hypertrophy, increased collagen synthesis and subsequent fibrosis [11]. The gene discussed is AGT; the disease is cardiac hypertrophy.