In human beings, TBX5 is highly expressed in embryonic andpostnatal hearts (Hatcher et al.,2000), and a number of TBX5 loss- or gain-of-functionmutations have been causally linked to HOS, including CHD and AF as well as cardiacblock (Al-Qattan and Abou Al-Shaar, 2015).Taken collectively, these findings suggest that genetically defectiveTBX5 enhances the susceptibility to CHD and AF in humans, andunderscore that TBX5 dosage must be precisely regulated to avoid heartdisorders. This evidence concerns the gene TBX5 and atrial fibrillation.