Sir,Recently, i read with interest the article of Javanmard et al., who reported that the aqueous level of vascular endothelial growth factor (VEGF) in non-proliferative diabetic retinopathy (NPDR) was not different compare to non-diabeticpatients, while soluble form of VEGF receptor-1 (sVEGFR-1) was lower in NPDR than non-diabetic subjects.[1]Several diabetic complications are related to imbalances between angiogenic and antiangiogenic factors.[2] Diabetic retinopathy is a microvascular diabetic complication and previous studies reported the role of angiogenic factors especially VEGF in this process.[3] It was shown that the VEGF/sVEGFR-1 ratio is a better indicator for angiogenesis process.[4] Although, in this study, the authors did not compare VEGF/sVEGFR-1 ratio between two groups, however, we should consider that the we cannot estimate the angiogenesis process NPDR patients solely by measurements of aqueous level of VEGF. In a recent paper, Waltenberger discussed regarding the VEGF resistance and angiogenic paradox in diabetes.[5] He indicated that the monocyte is a suitable cellular model for VEGF resistance. Although, the angiogenic response of VEGF is elevated in diabetes mellitus, however, the response to VEGF is reduced. On the other hand, it is important to distinguish between angiogenesis and arteriogenesis which may be involved in this paradox. According to this hypothesis, it seems that during the short period, arteriogenesis is reduced in diabetes mellitus due to VEGF resistance, however, in long-period, angiogenesis increases in spite of VEGF resistance the results of high and continuous stimulation of VEGF.[5] Increase in arteriogenesis is associated with collateral vessel formation, while, increase in angiogenesis is associated with diabetic retinopathy.[56] Thus, it seems that the role of VEGF and their receptors in proliferative or NPDR are more complex.