Interestingly, it has been observed that at molecular level, sustained therapy with β-blockers in HF is associated with resensitization of βARs, normalization of GRK2 levels and activity and as a consequence, β-blockers cause the upregulation of cardiac βARs (down-regulated in HF) increasing βAR signaling when they are activated (Leineweber et al., 2005). The gene discussed is GRK2; the disease is hydrops fetalis.