By contrast, fewer fluorescently labeled monocytes migrated through TNFα activated human dermal microvascular endothelial cells when they were isolated from PsA patients, compared to monocytes from patients with osteoarthritis, fibromyalgia or type-2-diabetes (as controls) – most likely due to a reduction in surface expression of the αMβ2-integrin required for stable/firm adhesion, explaining the reduced number of monocytes in the psoriatic joint, compared to RA (Neumüller et al., 2001). The gene discussed is TNF; the disease is rheumatoid arthritis.