Although ACEIs and ARBs have not shown a significant reduction in mortality and morbidity in patients with HFpEF [127,128], we have previously reported that macrophage accumulation, cardiac hypertrophy, and collagen deposition are significantly reduced with the use of AT1R antagonist, GLP-1 agonist, and curcumin (an anti-oxidant substance), which is consistent with the improved cardiac function in the rat models of Ang II infusion or TAC, suggesting that an interruption of Ang II/AT1 axis may delay the development of HFrEF [9,14,15]. The gene discussed is AGTR1; the disease is cardiac hypertrophy.