Finally, it should not be surprising that urinary proteins associated with ECM turnover (namely, MMP-2, TIMP-3, ECM1, TSP4, and MIA) emerged as the strongest readouts of concurrent tubular atrophy and interstitial fibrosis (i.e., high CI) in LN, given the direct role of these molecules in renal fibrosis. The gene discussed is THBS4; the disease is renal fibrosis.