In vivo studies with FcεRγ−/− MyD88−/− double knockout mice reveal lower arthritis severity scores than either of the single knockout strains or in WT mice, suggesting that both FcγR and MyD88-dependent pathways may contribute to the development of arthritis, and each pathway may take on a more prominent role when the other is inactivated. The gene discussed is MYD88; the disease is arthritic joint disease.