MCP-1 is known to contribute to the pathogenesis of experimental glomerulonephritis and it is present in the glomeruli of patients with AAGN.23, 24, 25 Indeed, urinary levels of this cytokine correlate with disease activity in AAV,26 and urinary MCP-1 has been proposed as a novel predictive biomarker in patients,27 perhaps supporting potential clinical application of SYK inhibition in AAV. This evidence concerns the gene CCL2 and anti-neutrophil cytoplasmic antibody-associated vasculitis.