In RA, abundant activation of individual members of TLR and IL1 families was already evidenced with a proposed role for exogenous TLR ligands in the disease onset (i.e., Proteus infection of urinary tract, Epstein-Barr virus, and parvovirus B19) and for endogenous ligands in self-sustaining of the inflammatory loop [5, 11]. Here, IL1B is linked to rheumatoid arthritis.