Atrial fibrillation (AF) is the most common arrhythmia, affecting more than 33 million people worldwide. AF is associated with increased risk of stroke and all-cause mortality and often co-occurs with or is caused by heart failure (HF). Because AF can often be asymptomatic and frequently underdiagnosed until a major adverse cardiovascular event occurs (eg, stroke, decompensated HF), identifying individuals at increased risk of AF (and AF recurrence1) creates an opportunity to intervene and reduce AF-related morbidity and mortality. Although several clinical risk prediction models for AF have been developed (eg, Cohorts for Heart and Aging in Genomic Epidemiology–Atrial Fibrillation [CHARGE-AF]),2 these risk estimates are highly dependent on age and limit the relevance for those with early-onset AF (EOAF; age ≤66 years). Indeed, in the US, the mean age for AF is 67 years for men and 75 years for women with 1 in 25 individuals having a diagnosis of AF before the age of 60 years.3 However, there is increasing awareness that individuals with EOAF may harbor pathogenic or likely pathogenic (P/LP) variants in cardiomyopathy and arrhythmia genes, which may represent unique risk markers to focus efforts on primary and secondary prevention of AF and AF-related cardiovascular disease (eg, stroke, HF).