Therefore, our findings may suggest that the onset of diabetic macular edema is associated with more elevated levels of angiogenic factor, inflammatory cytokines and chemokines released by macrophages, neutrophils, and endothelial cells, which are activated by four classic pathways: the polyol pathway, increased advanced glycation end-product (AGE), protein kinase C (PKC) activation, and the superoxide pathway [23]. Here, PRRT2 is linked to diabetic macular edema.