Pluripotent stem cells (PSC) in the bone marrow give rise to haemangioblasts (HA), with the potential to differentiate into either haematopoietic stem cells (HSC) or endothelial cell precursors (EPC; green). Mobilisation of EPC from the bone marrow is upregulated by many factors, including vascular endothelial growth factor (VEGF), erythropoietin, angiopoietin-1, and colony-stimulating factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF). In rheumatoid arthritis (RA), these cells appear to traffic to RA synovium at an enhanced rate, incorporating into blood vessels and giving rise to increased vascularity – thereby reducing the potential for revascularisation of ischaemic areas. Angiogenesis in the synovium is also VEGF dependent. As a consequence, circulating EPC numbers are reduced in RA and may lead to increased cardiovascular mortality.