It is speculated that factors causing podocyte damage in LP are similar to those contributing to MCD or primary FSGS,[1] which may include but may not be limited to aberrant T cell functions with alternatingly produced cytokines and lymphokines as proposed in MCD,[26] or some circulatory factors[27–29] such as soluble urokinase plasminogen activating receptor (suPAR),[30] as proposed in primary FSGS. The gene discussed is PLAUR; the disease is focal segmental glomerulosclerosis.