Two caveats when extending these findings to CaMKII hyperactivity in normal or failing myocytes are: (1) the β2a subunit is probably a lesser component of LCCs in non-diseased hearts, although its expression may be increased in heart failure (Hullin et al., 2007), and (2) the slowed inactivation in this study also increased total Ca2+ influx without destabilizing the AP. The gene discussed is CAMK2G; the disease is heart failure.