The fact that CD6 was preferentially expressed by all T cells, as well as by a small subset of mature B cells (B1a cells) involved in the production of low affinity polyreactive autoantibodies, soon led to early though discontinued attempts to treat certain autoimmune disorders (e.g., rheumatoid arthritis, psoriasis, and multiple sclerosis) using mouse anti-CD6 mAbs (2). This evidence concerns the gene CD6 and rheumatoid arthritis.