Therefore, to assess whether the down-regulation of KATP channels that we have demonstrated in the hearts of TAB mice may contribute to injury and further heart failure progression, and whether resistance to injury in the presence of CaMKII inhibition can be attributed to increased KATP channel expression, we assessed ischemia-reperfusion injury in isolated non-failing hearts from WT compared to the AC3-I, Kir6.2-KO and AC3-I/Kir6.2-KO genetic mouse models (Fig 6A). Here, CAMK2G is linked to heart failure.