This model has previously been established in preclinical cardiac transplant models as a method to study chronic rejection without immunosuppression because all allografts will develop vasculopathy.[24] ANA was used as a marker for antibody production because the minor MHC mismatch between Bm12 and C57/Bl6 (3 amino acids) does not result in alloantibody production, but rather autoantibody.[25] Post-transplant treatment with APRIL/BLyS blockade resulted in a significant reduction of serum ANA (p<0.0001) (Fig 1). This evidence concerns the gene TNFSF13 and vascular disorder.