However, with chronic heart failure, agonist-occupied βARs are stabilized in an active conformation that is phosphorylated by G protein-coupled receptor kinase (GRK); GRK-phosphorylated receptors then recruit β-arrestin, an adapter protein that acts to both sterically interdict βAR-G protein interactions and scaffold binding partners that trigger a second wave of signaling to Gs-independent growth regulatory responses such as extracellular-signal regulated kinase (ERK) and AKT (1, 2). Here, CTBP1 is linked to congestive heart failure.