Further, using an alternative autoimmune model, collagen-induced arthritis, Okabe et al. demonstrated that Sts-2-/- mice were significantly more susceptible to autoimmune induction than wild-type or Sts-1-/- animals, a finding that correlated with the observation of increased numbers of IL-2-producing splenic CD4+ T cells in Sts-2-/- vs. WT or Sts-1-/--challenged animals [26]. This evidence concerns the gene UBASH3A and arthritic joint disease.