Finally, we show that GSDMD may mediate inflammation via packaging and release of pro-inflammatory cytokines, such as IL-1β via EVs in addition to release through transmembrane pores or after membrane rupture, and that impairing GSDMD function using RNAi or blocking EV release in pyroptotic cells may pose a therapeutic opportunity for reducing IL-1β release and targeting inflammation in retinal degeneration. This evidence concerns the gene IL1B and retinal degeneration.