Sultana and Bishayi have used to neutralize or selectively inhibit TNFR1 or TNFR2 in a model of Staphylococcus aureus-induced septic arthritis; authors showed that the levels of pro and anti-inflammatory cytokines were modulated via the NF-kB and JNK signalling, which favored an increase of iNOS and RANKL and reduced recruitment of phagocytes at the site of inflammation, and subsequently decreased the generation of ROS and septic arthritis [90]. This evidence concerns the gene TNFRSF1A and bacterial arthritis.