In the tight-skin mice, a genetic model of human SSc, the CD19 signaling pathway appeared to be constitutively activated [6,7] and the loss of CD19 expression significantly up-regulated surface IgM expression, completely abrogated hyper-γ-globulinemia and autoantibody production, and also inhibited IL-6 production [7]. The gene discussed is CD19; the disease is systemic sclerosis.