However, the notion that cardiac β1AR signaling can turn cardioprotective in the failing heart goes directly against the consensus that selective cardiac β1AR downregulation, a molecular hallmark of chronic human HF, serves as an adaptive homeostatic process employed by the failing myocardium to shield itself against the chronic catecholaminergic stress in HF, which results from the chronically elevated SNS activity that accompanies and aggravates human HF [2]. This evidence concerns the gene ADRB1 and hydrops fetalis.