Introduction - In spite of scientific progress, much remains to be discovered about the genetic basis of human disease. Of the approximately 20,000 genes identified in the human genome to date, only 30% have been associated with disease, providing an opportunity to fill this knowledge gap by predicting genes likely to be associated with a given disease. - The hubs of molecular interaction networks, like busy interactions in road networks, provide one way of assessing the importance of a node or location. We propose a new method that nominates candidate genes for a disease by finding nodes that act as hub to a greater degree in the disease's subnetwork than in the entire network. Methods - Starting with a list of disease-associated genes (seeds), and a interaction network that includes metabolic, protein-protein, and transcription-factor interactions, we built a disease-specific subnetwork by generating all shortest paths between pairs of seed genes, counting the number of times each node appears on a path. Betweenness centrality (a measure of traffic through each node) was computed for each node in the subnetwork, and for the same nodes in the complete network. - The node count and two betweenness measures formed the input to a set of algorithms designed to separate the disease-specific nodes from their all-disease background. Combinatorial optimization was used to find the best choice of algorithm and measure thresholds by scoring each with the average rank of the disease's seed genes. Results - We performed two kinds of validation. First, the distribution of a disease's known seeds in the node scores was analyzed. More than 50% of all seeds occurred in the top 11th percentile of the list for Schizophrenia, showing strong enrichment of disease-related genes. Of the top 5 genes on this list not already known to be associated with Schizophrenia, 3 had been previously connected to Autism, Brain Diseases, or other neurological disorders in previously published scientific literature. Second, a list of 244 newly discovered genes related to Schizophrenia and not used for training was scored using our method. Of the 89 genes that appeared in our interaction network, 48% appeared in the top 18% of our ranked scores, once again demonstrating significant enrichment. Conclusion - We have presented a method to propose new disease-gene associations from known associations and a large molecular interaction network by using network properties to find disease-specific hubs. Our method is an effective way to make predictions of novel candidate disease genes for experimental validation.