Atrial fibrillation (AF) is a consequence of a complex interplay of genetic, epigenetic and environmental factors. In addition, AF is a major contributor to stroke, heart failure, and mortality. Several family studies have shown a strong polygenetic predisposition for AF but, so far, most of the linkage analysis and candidate gene studies have discovered only monogenic, rare, deleterious mutations. While research in human genetics has moved from monogenic to oligogenic to complex diseases, its pharmacogenetics branch has followed, usually a few years behind. The present paper reviews the potential contributions of genetic approaches to AF.