Pulmonary veins (PVs) and left atrium (LA) are the most important AF triggers and substrates.15, 16, 17 Calcium dysregulation plays a critical role in the occurrences of AF and PV arrhythmogenesis.18, 19 The activation of Na+/Ca2+ exchangers (NCXs) induces delayed afterdepolarizations (DADs) and increases PV arrhythmogenic activity.18 Protein kinase C (PKC)‐mediated signalling plays a vital role in NCX activation.20 H2S was known to activate PKC,21 thus H2S may increase INCX and increase PV arrhythmogenesis leading to AF genesis. This evidence concerns the gene SLC8A1 and atrial fibrillation.