Given that the protection from K/B×N serum transfer arthritis afforded by Ptpn22−/− mice was larger than that of any individual SFK (Hck, Fgr, or Lyn) (41), it is interesting to speculate that PTPN22 may contribute to regulating several SFKs, as well as other potential substrates. The gene discussed is HCK; the disease is arthritic joint disease.