Tissue hypoxia in the rheumatoid joint results in increased VEGF messenger ribonucleic acid (mRNA) stability [16] and enhanced VEGF gene transcription through the binding of hypoxia-inducible transcription factors such as hypoxia-induced factor-1 (HIF) and HIF-2 that are overexpressed in the synovial lining and stromal cells of RA patients relative to synovial tissues from individuals without arthritis [17]. Here, VEGFA is linked to arthritic joint disease.