The critical role of the GC in progression of allograft vasculopathy in our model most likely reflects its role in producing long-lasting alloantibody responses (60), and it is notable that the LLPC subset (that can potentially produce antibody for the life of the individual) was evident in the bone marrow of the SAP-replete group, but not in the SAP-deficient group. The gene discussed is SH2D1A; the disease is vascular disorder.