Nonetheless, independent of its precise mechanism of action on these channels, an emerging notion is that excessive CaMKII activity is detrimental for cardiac performance, and the potential salutary effect of blocking its chronic effects appears worth pursuing since its action on RyR2s and InsP3Rs might prevent both Ca2+-mediated arrhythmias and Ca2+-dependent activation of hypertrophic gene programs. The gene discussed is CAMK2G; the disease is cardiac arrhythmia.