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. The gene discussed is PRRT2; the disease is atrial fibrillation.