 Absence of sarcKATP, in addition to attenuating the benefits of IPC, significantly impairs the myocyte's ability to properly distribute Ca2+, decreasing sensitivity to sympathetic nerve signals, and predisposing the subject to arrhythmia and sudden death.Similarly, sarcKATP regulates vascular smooth muscle tone, and deletion of the "kir6.2" or "sur2" genes leads to coronary artery vasospasm and death.Upon further exploration of sarcKATP’s role in cardiac rhythm regulation, it was discovered that mutant forms of the channel, particularly mutations in the SUR2 subunit, were responsible for dilated cardiomyopathy, especially after ischemia/reperfusion.