Most of the pathophysiological effects of Aldo in the heart and vessels, which can cause essential hypertension and trigger cardiac hypertrophy, fibrosis, and adverse remodeling, are thought to result from MR activation, whereas several studies suggest that GPER activation may actually be beneficial in the myocardium, partly due to activation of antiapoptotic mediators, such as Epidermal Growth Factor Receptor (EGFR) and extracellular signal-regulated kinase (ERK)1/2 [2,3,4,5,6,7]). The gene discussed is EGFR; the disease is hypertensive disorder.