Complex phenotypes such as lifespan, disease susceptibility, and mutation penetrance vary substantially even among isogenic individuals. The molecular determinants behind this variation have long been sought, along with the ability to predict how one individual will differ from another. In Caenorhabditis elegans, variation in lifespan and mutation penetrance among nominally isogenic individuals has recently been linked to differences in expression of molecular chaperones. These expression differences are heritable, implying a stable epigenetic or unstable genetic source. We propose copy number variation in ribosomal RNA genes as an underlying, unexplored genetic cause of phenotypic variation. Ribosomal RNA genes (rDNA) exist as tandem gene arrays in all eukaryotes, and their repetitive nature predisposes them to instability and thus copy number variation among individuals. Differences in rDNA copy number indeed exist among laboratory N2 worms only ten generations removed from a common ancestor. rDNA copy number is known to associate with global gene expression in flies and humans. rDNA also associates with genome integrity and replicative lifespan in yeast. Furthermore, the nucleolus itself, which is comprised of rDNA, is a major hub of stress response and protein homeostasis. Despite its obvious biological significance, rDNA and its copy number variation are understudied, due largely to the inherent technical challenges involved in genotyping repetitive DNA. We have addressed this problem by developing a high-throughput technology to genotype rDNA copy number in C. elegans, employing molecular inversion probes to count repeat units. This cost-efficient and universally applicable method provides rDNA copy number estimates that agree with whole genome sequencing-based estimates. Facilitated by this technology, we have begun exploring the potential phenotypic consequences of rDNA copy number variation. Our preliminary data show an association between rDNA copy number and two different biomarkers of longevity. Our results suggest that rDNA copy number may be a contributor to phenotypic variation among nominally isogenic individuals. We provide a technology to make this class of genetic variation accessible for in-depth exploration of the phenotypic consequences of rDNA copy number variation in C. elegans as well as for future studies of aging and disease susceptibility in other organisms, including humans.