Genetic factors are fundamental in the molecular pathologic mechanisms of a number of auditory disorders that present throughout the lifespan. Historically, an understanding of the role of genetics in tinnitus has not been as straightforward because it can be viewed as a symptom of multiple diseases. Risk factors for tinnitus include hearing loss, aging, and noise exposure, most logically connecting its cause with environmental factors. This notion has been supported by a lack of heritability determined from early family-based questionnaire studies.1,2 In addition, previous studies that have primarily used genotyping in the pregenomics era have identified several candidate genes implicated in tinnitus (summarized by Lopez-Escamez et al3) that have thus far lacked replication, and a recent pilot genome-wide association study4 also did not reveal significant associations. Throughout the course of genetics research in tinnitus, it has become increasingly clear that the lack of significance may have been hampered by an underappreciation of the clinical heterogeneity and subtypes that are inherent in tinnitus, which may have profoundly clouded true significant associations.3