 Even with the ability to look at a person's entire genome, many people with genetic diseases remain undiagnosed. Previously, this was due to a lack of information, but now it's because there's so much new data that it's hard to tell what's meaningful. Genes can now be sequenced so quickly and cheaply that sifting through the data has become the biggest challenge. However, a group of American researchers has developed a way to make sense of it all. They've created a scoring system that can determine which genes actually cause a particular disease. The system works by looking at whether published evidence supports that certain changes in a given gene are the true cause of a condition. The group considered several factors, such as how many patients with mutations in the same gene are affected by the same disease, how many different mutations in the same gene cause a similar set of symptoms, and whether mutating a gene in cells and animals in the lab produces symptoms that mimic the human disease. By awarding a score for each category and adding these values, they can tell whether there is strong, moderate, or weak evidence relating a gene to a disease. To test the real-world utility of the system, the group scored new scientific findings and then reviewed records for more than 2,000 patients who previously underwent genetic screening. They found new diagnoses for more than 5% of previously unsolved cases. Based on this outcome, it is clear that enough new information has been published to finally provide many previously undiagnosed patients with information about the cause of their conditions, leading to improved care. These findings show that in the world of genome-based medicine, sequencing is just the first step. Being able to efficiently curate the vast amount of genetic information is just as important. With easily interpretable scores, doctors can more readily and accurately identify patients with new genetic diseases, shifting the focus from diagnosing these patients to helping them receive the best treatments.