The striking similarity of these findings to experiments employing prolonged isoproterenol exposure (Figures 1—4) supports that fragmentation of RyR clusters during HF results from increased activation of both CaMKII and PKA, likely as a consequence of the chronic β-AR stimulation that is well established in this condition (Ganguly et al., 1997). The gene discussed is RYR2; the disease is hydrops fetalis.