Mouse genetics is a powerful tool for discovering genetic factors influencing human pain sensitivity. However, many previous studies relied on mapping populations that lacked recombinatorial precision, resulting in pain-related quantitative trait loci (QTL) that are quite large, often spanning several megabases and containing numerous candidates. In order to improve genetic mapping efficiency, a cohort of approximately 300 Diversity Outbred mice was tested to identify novel genes associated with acute thermal pain sensitivity. Diversity Outbred mice offer increased genetic heterozygosity, allelic diversity, and recombinatorial precision compared to traditional mouse mapping populations, making them an ideal resource for high-resolution genetic mapping. The candidate pain gene Hydin, encoding axonemal central pair apparatus protein, was identified in a 2.5 Mbp QTL region. The plausibility of Hydin's role in pain response was assessed by combining annotation data from publicly available sources with genetic network analysis tools to visualize known and predicted functional relationships between Hydin and known nervous system genes. Our findings suggest a role for Hydin in pain sensitivity, possibly through the involvement of the cerebrospinal fluid-choroid plexus system.