The mechanism underlying the increased risk for AMD development in patients with polymorphisms associated with Tgfbr1 (Fritsche et al., 2013) may relate to decreased levels of TGFβ signaling from the retinal environment to microglia in the AMD retinas, consequently shifting microglia from a homeostatic physiological state to a pathological state (Figure 10). This evidence concerns the gene TGFBR1 and age-related macular degeneration.