AhR-/- mice show loss of RPE cell tight junctions; accumulation of RPE cell lipofuscin; basal laminar, linear-like deposit material; Bruch’s membrane thickening; progressive RPE and choroidal atrophy; and choroidal neovascularization [8,9,24] Consistent with this, treatment with the AHR agonist significantly lowered diabetes-mediated leukocyte retention, oxidative stress and inflammation in streptozotocin-induced retinopathy, demonstrating that AHR could potentially represent a novel therapeutic target for diabetic retinopathy [14]. This evidence concerns the gene AHR and retinal disorder.