Combined with the fact that putative causal variants were enriched in binding sites of TBX5, NKX2-5 and GATA4 (Fig. 4i and Supplementary Fig. 9e), these results suggested that perturbation of transcriptional regulatory networks consisting of TFs and their targets, plays a critical role in the genetics of AF. This evidence concerns the gene TBX5 and atrial fibrillation.