Epilepsy gene panels, querying a selection of known genetic etiologies using next-generation sequencing technologies, have emerged as the first-tier genetic test in clinical practice. Most gene panels are performed through commercial laboratories. In contrast to publicly funded research, data generated from commercial laboratories are typically not open to the scientific and medical community. It is currently unclear how many genetic tests for epilepsy are performed each year, but many diagnostic companies claim to have genotyped several thousand patients. This raises the concern that fundamental insights into the genetic architecture of the epilepsies that are important for the development of novel therapies are prevented by siloing of data and proprietary interests. In a current publication by Lindy and collaborators published in the current issue of Epilepsia,1 a large US-based diagnostic laboratory makes some of their data accessible by reporting the results of more than 8500 epilepsy gene panels. The analysis reported is unique given its size: this study is one of the largest epilepsy genetics study to date,2 dwarfing comparable exome or gene panel studies by a factor of 5 or more.3, 4 Despite the absence of detailed clinical data, limited to the information provided by ordering physicians, the current study allows for some interesting insights. First, pathogenic or likely pathogenic variants are found in approximately 15% of patients. This rate is at the lower end of what has been reported in prior studies,5-7 but provides a robust estimate given the number of patients. The current study was unable to assess the final clinical interpretation, and it should be emphasized that classification of a variant as “pathogenic” does not provide a diagnosis by itself. Variant interpretation is based mainly on laboratory data, and a proportion of variants are reclassified when interpreted in the appropriate clinical context.8, 9 Therefore, some of the results need to be interpreted with caution, as a patient's clinical presentation is important in making the final diagnosis for many genes. Second, the authors find that only a few genes account for most explanatory findings. SCN1A and KCNQ2 alone explained almost 40% of “positive” patients, and only 22 genes contributed significantly to the diagnostic rate. In contrast, 16 genes did not have a single positive case. This may be due to the rarity of the associated conditions as in the case of CSTB and GOSR2, genes for progressive myoclonus epilepsies.10, 11 Alternatively, the tested genes may not be true disease genes, which may be the case for EFHC1, SRPX2, ATP6AP2, or CACNB4. These genes were once thought to be candidate genes, but further evidence has been lacking or conflicting.12, 13 In both cases, the low yield suggests that these genes are not necessary, or perhaps even suitable, to be included in a first-pass diagnostic test. Overall, the study by Lindy et al highlights the frequency of common genetic causes of epilepsy as well as a variant spectrum and segregation patterns, providing an important backdrop for future studies into the full range of disease presentations. Finally, disease-causing variants in the 7 most commonly identified genes (SCN1A, KCNQ2, CDKL5, SCN2A, PRRT2, PCDH19, and STXBP1) account for almost 900 patients. This number alone emphasizes that “rare is common,” demonstrating the pressing need to develop broad-based diagnostic strategies to reach the large group of patients for whom testing would be beneficial as well as targeted treatment strategies for patients with genetic epilepsies. I have no conflicts of interest to disclose. I confirm that I have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.