Amit et al.36 demonstrated in a pig model that APD could be prolonged via the epicardial gene painting of an AD vector encoding a dominant negative mutation of KCNH2. By interrupting the alpha subunit of the IKr channel in the gene-treated pigs, the investigators found an increase in the APD, resistance to burst pacing-induced AF, and increased conversion from AF to sinus rhythm. Here, KCNH2 is linked to atrial fibrillation.