Sex steroids such as estrogen and testosterone are key mediators of angiogenesis. They are implicated in both physiological and pathological angiogenesis such as during the menstrual cycle, wound healing, and cancer growth and progression. Sex steroids regulate many aspects of angiogenesis through both classic genomic signaling pathways which regulate gene expression and also rapid action nongenomic pathways. In this capacity, sex steroids are able to modulate endothelial and progenitor cell functions such as proliferation, migration, and attachment, which are all essential components involved in neovascularization. Since sex steroids are known to augment angiogenesis which is vital to tumor progression and growth, common treatment of hormone-responsive tumors is through sex steroid receptor antagonists. Due to the involvement of sex steroids in necessary physiological functions as well as the potential to promote pathological angiogenesis, it is fundamental that the mechanisms behind sex steroid-mediated neovascularization are understood.