Our current findings, in the context of those from SLE, suggest that analyses of B cell signaling in more defined subsets such as DN2 (CD20++CD27negIgDnegCD11c+) or activated naïve B cells (CD20++CD27negIgD+CD11c+) will provide greater insight into the immunopathogenesis of RA. This evidence concerns the gene ITGAX and rheumatoid arthritis.