miR-1 levels were reduced in the left atrium of AF patients, resulting in increased inward rectifier potassium channel (Kir2.1) [162], and miR-1 was found to accelerate shortening of the atrial effective refractory period (AERP) in a rabbit model, resulting in increased AF susceptibility by down-regulation of KCNE1 and KCNB2 [163]. This evidence concerns the gene KCNJ2 and atrial fibrillation.