Moreover, loss of PRRX1 was shown to shorten the action potential duration as well as effective refractory period in human atrial cardiomyocytes and zebrafish embryonic myocardium, forming a substrate vulnerable to AF (Tucker et al., 2017), which was further substantiated in a mouse model with deletion of the noncoding AF-associated genomic region (Bosada et al., 2021). This evidence concerns the gene PRRX1 and atrial fibrillation.