G1 also reduced cardiac hypertrophy, fibrosis, atrial natriuretic peptide, brain natriuretic peptide and β-myosin heavy chain, and the augmented oxidative stress and apoptosis induced by Ang II in mice, whereas GPER deficiency exacerbated the Ang II effects [291], suggesting potential benefits of G1 in alleviating cardiac hypertrophy and fibrosis in Post-MW. The gene discussed is GPER1; the disease is cardiac hypertrophy.