However, higher levels of vWf, MCP-1, and sVCAM-1 observed in patients with low disease activity exhibiting no further significant rises with an increase in disease activity may suggest a dissociation of pathways governing generalized and joint-specific inflammatory reactions from those responsible for endothelial activation and chronic inflammation within the vascular wall and that the presence of RA itself, rather than the magnitude of concomitant inflammatory activity, contributes to endothelial dysfunction. The gene discussed is VWF; the disease is endothelial dysfunction.