Accumulating evidence supports activation and/or increased expression of α9 as a key mechanism in the RA disease process [20, 32, 42] including α9 overexpression on FLS in rheumatic joints preceding the onset of arthritis [18, 19, 35], and the activation of α9 stimulating transformation of FLS into a pathologic state that includes hyperplastic and proinflammatory activity [33]. This evidence concerns the gene IGKV1D-22 and Arthritis.