Schuster et al. (2016) reveal that overexpression of ERβ in mice reduced myocardial fibrosis and collagen I/III deposits, improving cardiac function. Inversely, Skavdahl et al. (2005) detect basal cardiac hypertrophy in female mice deficient for ERβ, confirming the important role of this receptor for cardiac hypertrophy development in females. Moreover, imbalance between ERα and ERβ is reported in diabetic women and may explain the loss of estrogen cardioprotection regarding myocardial hypertrophy and fibrosis in DCM (Wells et al., 2005). The gene discussed is ESR2; the disease is familial dilated cardiomyopathy.