Previous studies reported that HO-1 was upregulated in tubular epithelial cells of the human kidney in various renal diseases, epithelia are more susceptible to oxidative stress due to the lack of this critical enzyme,[5] and HO-1 deficiency promotes epithelial-mesenchymal transition and renal fibrosis.[6] However, whether overexpression of HO-1 is beneficial or detrimental in kidney disease is unclear. Here, HMOX1 is linked to renal fibrosis.