The role of the vitreous and vitreomacular interface on the development and response to treatment in DMO has been speculated to arise from micro and macro traction, a reservoir for pro-inflammatory factors ‘trapped’ in the retina and as a barrier to therapeutic anti-VEGF drug diffusion [9, 11, 12] VMIA has also been suggested to be a marker of more severe baseline activity of diabetic retinopathy and to occur in eyes with more limited visual potential [1]. This evidence concerns the gene VEGFA and diabetic retinopathy.