Our study has several limitations: There is no direct interaction between VEGFR-3 and TLR7 activation, unproven in situ autoantibody production by TLO-resident B cells, reliance on a single animal model for lupus nephritis, short-term treatment and lack of functional lymphatic readouts and a small number of the human cohort (n = 22) for evaluation the association of lymphatic vessel expression with histopathological activity and serologic markers in human lupus nephritis. The gene discussed is TLR7; the disease is lupus nephritis.