The ability of VIP to modulate Th17 or Th1 effects in RA is not restricted only to its effect on CD4 T lymphocytes since VIP counteracts the enhancing effect of proinflammatory molecules on IL-22R, IL-17R, and IL-12 family of cytokines in FLS disfavoring the cross-talk between FLS and Th1/Th17 cells [49, 102]. The gene discussed is CD4; the disease is rheumatoid arthritis.