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However, long\u2010term treatment with such anti\u2010VEGF\u2010A therapies may impair physiological functions of the choriocapillaris and retina for which VEGF\u2010A is needed. Moreover, disease progression can occur despite continuous anti\u2010VEGF\u2010A treatment. Thus, novel therapies for NV\u2010AMD are urgently needed that target specifically disease\u2010associated mechanisms without impairing growth factors and cellular pathways that are required for homeostatic functions of the retina and choroid. Inhibiting the inflammatory pathways that promote CNV would be such a promising novel approach that would likely not interfere with the normal functions of healthy retinal and choroidal cells. In this context, the inflammasome, a proinflammatory protein complex that promotes pathologic angiogenesis largely through generation of IL\u20101\u03b2 and which has been reported to be activated in AMD, has become an area of much interest in the AMD field. However, most studies have focused mainly on the NLRP3 inflammasome in retinal pigment epithelial cells (RPE), and conflicting findings have resulted in an unclear picture of the role of the inflammasome for AMD pathogenesis. Recent data suggest that inflammasome activation in activated macrophages and retinal microglia but not in RPE cells promotes CNV. Furthermore, inflammasome activation can occur in CNV macrophages and microglia despite lack of NLRP3. 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