This may be explained by the notions that 1) LLT1 expression can be induced in B-cells and DCs following their in vitro stimulation with TLR ligands [13,14], 2) the expression of several TLR ligands [21–23] was previously found to be increased at RA inflammatory sites, 3) several pro-inflammatory cytokines (particularly Th1 cytokines such as IFN-γ) implicated in RA pathogenesis amplify the TLR-induced cellular activation, 4) T-cells [24], B-cells [25], monocytes [26] and neutrophils [27] in RA SF are characterized by an activated phenotype. The gene discussed is IFNG; the disease is rheumatoid arthritis.