Using a VEGF-based transgenic mouse model it was observed that NLRP3 inflammasome activation and secretion of its effector cytokine IL-1β promoted AMD-associated pathologies, including RPE barrier breakdown and CNV lesion formation [52], possibly through the strong angiogenic properties of IL-1β [58,59,60,61,62,63]. The gene discussed is NLRP3; the disease is age-related macular degeneration.