To ascertain and identify the cause for both inflammatory and pathogenic Th17 cell presence in RA, we then examined for FasL expression in RA IFN-γ+(Th1), IL-17A+(Th17) and IFN-γ/IL-17A+(Th1/Th17) cells from long-lived memory or effector compartments (Figure 3A). This evidence concerns the gene FASLG and rheumatoid arthritis.