Atrial fibrillation (AF), the most prevalent cardiac arrhythmia, affects more than 60 million people worldwide and is associated with increased risk for stroke, heart failure, and dementia, justifying it as a major public healthcare burden2,3. AF is characterized by irregular and often abnormally fast heart rates4,5. Over the last decade, tremendous progress has been made in understanding the genetic architecture of AF6–8. Genome-wide association studies have identified over 140 common loci associated with AF, while family-based studies have implicated rare variants primarily encoding ion channels9,10. Although AF has been traditionally classified as a ‘channelopathy’, variants in myocardial sarcomeric proteins such as titin have been increasingly associated with familial or early-onset AF11,12.