To assess the effects of FcγR deficiency on prevalence of arthritis after B. burgdorferi infection, we determined the number of joints that had evidence of inflammation in WT and MyD88−/− mice for comparison with FcεRγ−/− and the double knockout FcεRγ−/− MyD88−/− mice (Table 1). This evidence concerns the gene FCGR2A and arthritic joint disease.