In this context, miR-30a up-regulation reduces AF-induced myocardial fibrosis by targeting snail family transcriptional repressor 1 (SNAIL1) [163], whereas, miR-30c overexpression attenuates atrial fibrosis induced by TGF-β1, by targeting transforming growth factor beta receptor 2 (TGFβRII) [164], being both of them down-regulated in AF patients with an increase of fibrotic tissue. This evidence concerns the gene SNAI1 and atrial fibrillation.