Atrial fibrillation (AF) is the most common arrhythmic disorder, and currently affects nearly 3 million Americans, 8.8 million Europeans, and an estimated 30 million individuals worldwide. The clinical risk factors for AF are numerous, with age, sex, hypertension, obesity, and ischemic heart disease among the most prevalent. Over the last ten years, a preponderance of evidence also suggests a large genetic contribution to AF. The earliest report of familial AF dates to the early 1940s1. Since then, it has become apparent that AF in referral populations2,3 and in the community is heritable4,5. Indeed, having a family member with AF is associated with a 40% increased risk for the arrhythmia6. Once the heritability was recognized, traditional genetics techniques for the discovery of rare, monogenic causes of AF were used to identify the initial AF genes. These studies in turn, informed candidate gene screening in AF cohorts. To identify additional sources of heritability for AF, large-scale analyses of common variation through genome wide association studies (GWAS) has recently yielded data identifying risk loci in many regions of the genome. In spite of these advances, the combination of these techniques has, as yet, failed to completely identify the heritability of AF in the population. It is the goal of this review to examine the previous studies on rare variants, address the findings of the recent GWAS studies, and describe future avenues towards defining the heritability of AF.