Abnormally enhanced automaticity of working cardiac myocytes can be induced by increased extracellular K + concentration (resulting e.g. from ischemia), reduced expression/activity of potassium channels or increased expression/activity of ion channels responsible for inward depolarizing current (e.g., HCN4 channel, as we showed before in the post-MI setting5, although this mechanism is regarded as less important source of VEBs than afterdepolarizations. This evidence concerns the gene KCNA3 and ischemia.