Liang et al. (2014) showed that loss-of-function mutations of TASK-1 lead to increased susceptibility to develop AF in the presence of pro-arrhythmic stimuli and Harleton et al. (2015, 2013) observed a phosphorylation dependent TASK-1 dysregulation in a canine model of AF, further underlining its role in AF. Here, KCNK3 is linked to atrial fibrillation.