Regulation of angiogenesis occurs in the context of particular microenvironments and is governed by a sensitive balance between angiogenic and anti-angiogenic mediators. Under normal physiologic conditions, the expansion of existing blood vessels is held in check suggesting that homeostasis is maintained by a predominance of angiostatic factors. In the rheumatoid arthritis joint, it is probable that the expansive and tumor-like synovial pannus that invades cartilage requires additional nutrients and oxygen. In the face of these demands, there is likely a shift in the balance such that angiogenic mediators predominate leading to neovascularization, a hallmark of rheumatoid arthritis. Chemokines are a subset of cytokines that primarily mediate physiologic and pathophysiologic leukocyte trafficking during inflammation and immune cell differentiation. Chemokines are also fundamental participants, along with a variety of other factors, which regulate angiogenesis. Within the CXC family of chemokines, there is functional discrepancy, where some family members are angiogenic and others are angiostatic. Moreover, the expression of several chemokines has been well documented in rheumatoid arthritis synovial tissues and fluids. This review will discuss what is known about the role of specific chemokines in the regulation of angiogenesis with particular emphasis on those chemokines likely to participate in rheumatoid arthritis.