KCNN4 and myocardial infarction: As already mentioned in section 4.1, in the mouse MI model KCa3.1 activation in recruited macrophages facilitates Ca2+ influx and causes APD prolongation of cardiomyocytes which are connected to these macrophages via gap junctions, ultimately resulting in prolonged QTc duration and enhanced susceptibility to ventricular arrhythmias (Figure 2D) (Fei et al., 2019).