The induction and maintenance of joint pain are associated with intense CXCL1-mediated neutrophil influx and production of hyperalgesic mediators, such as IL-1β (Cunha et al., 2010; Sachs et al., 2011; Amaral et al., 2012), and blockade these mediators have been described to suppressed joint pain and damage in murine model of arthritis (Williams et al., 2000). This evidence concerns the gene IL1B and arthritic joint disease.