FSGS is a life‐threatening nephropathy and podocyte injury such as EMT plays a critical role in the disease progress.[7, 28, 33] Although Btg2 mutation induces hypertension and proteinuria in female high‐salt diet‐fed rats, deletion of Btg2 shows no significant phenotype in the mouse kidney.[34, 35] In this study, we found that Btg2 was significantly upregulated in glomerular cells, especially in podocytes, in patients and mice with FSGS. This evidence concerns the gene BTG2 and focal segmental glomerulosclerosis.