In 2007, Tuo et al reported that the combined deletion of chemokine Ccl2 and Fractalkine receptor Cx3cr1 on C57BL/6N genetic background (i.e., CCL2−/−CX3CR1−/− mice) resulted in an early onset of spontaneous retinal degeneration with AMD-like features such as RPE alteration, photoreceptor damage and A2E elevation [30], and the mouse has been considered as a valuable model of AMD [46]. The gene discussed is CX3CR1; the disease is age-related macular degeneration.