Work in relevant in vitro (eg, cardiomyocyte/neuronal cultures derived from stem cells from patients with XLI) and in vivo models (eg, Sts-deficient mice), in combination with more focused clinical analyses in Xp22.31 deletion carriers guided by the preliminary results presented here, should clarify the physiological, cellular and molecular mechanism(s) through which genetic variants at Xp22.31 affect risk of AF and other relevant medical conditions. This evidence concerns the gene STS and atrial fibrillation.