Endometriosis is an inflammatory gynecological condition that affects 6-10 percent of the general female population. In this disease, the endometrium implants outside of the uterus, in the peritoneal cavity. This can lead to chronic pelvic pain, painful menstrual bleeding, and infertility. The cause of endometriosis remains unknown and the pathology must be understood before new treatments can be made available. This project was thus developed to examine disease formation through a multidisciplinary perspective. Previous work from the Eyster laboratory has shown that gene expression is altered substantially in endometriosis lesions compared to normal endometrium. The establishment of a mouse model allows us to study the development of endometriosis and to determine the effects of specific genes known to be up-regulated in endometriosis. As an addition to the in vivo studies, a mathe- matical model has been developed to understand and analyze the dynamics of some of the quantifiable elements of endometriosis. The hybrid discrete-continuum model using partial differential equations was used to analyze the effects of specific genes on disease development based on gene ontologies. Taken together, the biomedical research and the mathematical representation provide both predictive insight and a means of experimental verification of the involvement of specific genes in the development and progression of endometriosis.