Our here presented findings suggest that non-HLA-directed GPCR/PAR1-activating regulatory autoantibodies (RABs) that are found in KTx-IgG from transplant patients with vasculopathy can trigger substantial TNF-α production from ECs and myeloid cells, and KTx-IgG from patients with vasculopathy potentiates the response to the natural activator thrombin. The gene discussed is F2R; the disease is vascular disorder.