The observation that glomerular but not serum TNF levels correlated with loss of eGFR in this study suggested that, regardless of the nature of one or more circulating factors present in the serum of patients with FSGS, the renal intrinsic activation of the TNF pathway contributes to disease pathogenesis and/or progression in FSGS[19], or that multiple circulating factors contribute to the pathogenesis of primary FSGS and thus correlations between a single circulating factor and a clinical phenotype might not always be evident[20]. The gene discussed is TNF; the disease is focal segmental glomerulosclerosis.