In rodents, Adriamycin (ADR) can induce rapid podocyte injury featured with massive foot process effacement and glomerulosclerosis, which serves as a model of FSGS.[25, 26] In the present study, we investigated Btg2 expression and its role in ADR‐induced FSGS by podocyte‐specifically deleting Btg2. This evidence concerns the gene BTG2 and focal segmental glomerulosclerosis.