Since a previous study found that disrupting tight junction proteins in RPE cells leads to the initiation of EMT [29], we examined the junctional proteins in our mouse model and found that loss of Akt2 in the RPE attenuated diabetes-induced decreases of the adherens junction protein E-cadherin and tight junction proteins ZO-1 and Occludin (Fig. 4E–G). The gene discussed is OCLN; the disease is diabetes mellitus.