After binding to HMOX1, Stannsoporfin can inhibit its activity; prevent heme from entering the active site; reduce harmful metabolites; alleviate oxidative stress; relieve cell damage; protect mitochondrial function; maintain energy metabolism; and indirectly block the vicious cycle of “oxidative stress–cytokine release–immune cell infiltration”, reduce NF-κB activation, decrease the expression of cytokines, inhibit the recruitment and activation of immune cells, relieve retinal inflammation and edema, and delay the progression of diabetic retinopathy [55]. Here, NFKB1 is linked to inflammatory response.