However, in different organs, other anti-fibrotic mechanisms activated by NRF2 are advanced to assist the two main factors above in relieving fibrosis, downregulation of JAK2/STAT3 in hepatic fibrosis, inhibition of RIPK3 induced mitochondrial dysfunction in myocardial fibrosis, epithelium mesenchymal transition in pulmonary fibrosis and the balance of gut microbiota in intestinal fibrosis for instance (Figure 2). This evidence concerns the gene NFE2L2 and pulmonary fibrosis.