Interestingly, this study also demonstrated that Cpa3Cre/+ mice developed full antibody-mediated arthritis with no significant difference compared to Cpa3+/+ mice, suggesting that MCs are dispensable for development of arthritis and that c-kit mutation rather MC deficiency was responsible for disease resistance in KitW/W-v strain [57]. The gene discussed is KIT; the disease is arthritic joint disease.