EGFR and hydrops fetalis: While β1ARs can also activate cardioprotective Gs-independent mechanisms via the recruitment of β-arrestin and transactivation of an epidermal growth factor receptor (EGFR) pathway that activates ERK1, chronic β1AR activation leads to a spectrum of changes (including cardiomyocyte hypertrophy/apoptosis, interstitial fibrosis, and contractile dysfunction) that contribute to the evolution of heart failure (HF)2, 3.