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 kidney disorder.