Various in vitro models of retinal degenerations, using mostly RPE and microglia/macrophages in culture, have shown increased gene and/or protein expression levels of IL-1β in response to oxidative stress and inflammatory stimulations such as 4-hydroxynonenal (HNE), an end product of lipid peroxidation (271), lipofuscin components including A2E (272–275), Aβ (276–278), lysosome destabilization (104), lipopolysaccharide (LPS)-stimulated microglia-conditioned medium (279), and complement components (31, 280, 281). The gene discussed is IL1B; the disease is retinal degeneration.