In this mouse study, sera from patients with recurrent FSGS, but not from those with non-recurrent FSGS or normal controls, activated β3 integrin activityin vitro, promoting cell motility and activation of the small GTPases cdc42 and Rac1, while inhibition of suPAR reduced β3 integrin activity and reduced podocyte motilityin vitro in addition to proteinuria reduction in these animals17. The gene discussed is CDC42; the disease is focal segmental glomerulosclerosis.