Chronic hyperglycemia, hypoxia, and release of inflammatory molecules (e.g., tumor necrosis factor, TNF-α, or Interleukin-1β, IL-1β) have a strong impact on retinal homeostasis by promoting on the one hand vascular dysfunction and pathological angiogenesis, both a cause of proliferative diabetic retinopathy, and on the other increased capillary permeability, with the associated production of hemorrhages and inflammatory exudate [14]. Here, TNF is linked to proliferative diabetic retinopathy.