Although, we could not examine the role of α2β1 integrin specifically in RA Th17 vs. Th1 cells, it is likely that a similar mechanism occurs in both populations since α2β1 integrin is a costimulatory molecule for both Th1 and Th17 (5–7), and as shown in Figure 1D, both Th1 and Th17 can be protected by anti-CD3+collagen costimulation since MTX-rescued cells are able to produce IL-17 and IFNγ to the same extent as control cells upon restimulation. The gene discussed is IFNG; the disease is rheumatoid arthritis.