Proliferative diabetic retinopathy (PDR) remains the leading cause of blindness among working-age individuals in developed countries (1). Diabetic macular edema (DME), another important event that occurs in diabetic retinopathy, is more frequent in type 2 than type 1 diabetes (2). Whereas PDR is the most common sight-threatening lesion in type 1 diabetes, DME is the primary cause of poor visual acuity in type 2 diabetes. Because of the high prevalence of type 2 diabetes, DME is the main cause of visual impairment for diabetic patients (2). In addition, DME is almost invariably present when PDR is detected in type 2 diabetes (3). Neovascularization caused by severe hypoxia is the hallmark of PDR, whereas vascular leakage caused by the breakdown of the blood retinal barrier (BRB) is the main event involved in the pathogenesis of DME (4,5). Although tight control of both blood glucose levels and hypertension is essential to prevent or arrest progression of the disease, the recommended goals are difficult to achieve in many patients and, consequently, diabetic retinopathy develops during the evolution of the disease. When PDR or clinically significant DME do appear, argon-laser photocoagulation is currently indicated, which the efficacy of has been widely demonstrated (6). However, the optimal period for laser treatment has frequently passed; moreover, it is not uniformly successful in halting visual decline. In addition, argon-laser photocoagulation is associated with moderate visual loss, some diminished visual field, reduced color vision, and reduced contrast sensitivity. The presence of these symptoms led to the prevailing thinking that laser treatment prevents vision loss but rarely results in visual improvement. Intravitreal corticosteroids have been successfully used in the eyes of patients with persistent DME and loss of vision following the failure of conventional treatment (i.e., focal laser treatment and attention to systemic risk factors). However, …