Obesity contributes to the development of HFpEF by increasing renal tubular sodium reabsorption and expanding plasma volume [1] with overproduction of aldosterone through two pathways: (1) renin angiotensin system (RAS) activation and increased aldosterone secretion from the adrenal cortex and adipocytes and (2) direct leptin stimulation of adrenal cortical cells [63]. The gene discussed is LEP; the disease is obesity disorder.