In this sense, activation of TLR2, TLR3, and TLR4 in FLS from RA patients exacerbated inflammatory Th1 and Th17 cell expansion both in cell–cell contact-dependent and inflammatory cytokine-dependent manner, which induced more IFNγ and IL-17 accumulation [10, 95]. This evidence concerns the gene IFNG and rheumatoid arthritis.