As CD9 de novo expression in glomeruli was observed in podocytes and PEC in human CGN and, given the recognized role of podocytes in the progression of crescentic lesions in CGN2,30–32, we then deleted Cd9 selectively in podocytes (Pod-Cd9lox/lox mice) by crossing Cd9-floxed mice with mice expressing CRE under the NPHS2 promoter (Pod-Cre mice)33. The gene discussed is CD9; the disease is childhood gender nonconformity.