In the diabetic retina disruption of fractalkine (FKN) signaling induces fibrin(ogen) deposition, increased production of IL-1b by microglia, vascular and neuronal damage. But, how FKN and its receptor, CX3CR1, regulate microglia activation and retinal pathology is unknown. In humans, two single nucleotide polymorphisms in the CX3CR1 locus (hCX3CR1-I249/M280) that show defective binding to FKN, play a key role in inflammation during diabetes. Notably, assessments of the effect of hCX3CR1-I249/M280 in an animal model revealed that express