An additional modulator of Kv1.5 is nitric oxide (NO), a long-established, biologically active signalling molecule in the cardiovascular system as well as other tissues.37, 38, 39 NO regulates Kv1.5 via nitrosylation and activation of cGMP,30 an effect which is of potential importance in the context of AF, given the important role of this channel in atrial electrical activity, and also the fact that NO bioavailability is reduced in AF and NO synthases (NOSs) can become uncoupled, leading to superoxide formation.38, 40, 41. Here, KCNA5 is linked to atrial fibrillation.