Thus, it can be envisioned how, in AMD, AAbs directed against HSPB4/CRYAA could compromise its functions and contribute to AMD-promoting RPE damage and loss, possibly by promoting formation of the intra- and/or extra-cellular aggregates that are seen in AMD and that can lead, independently of autophagy compromise, to NLRP3 inflammasome activation [136]. The gene discussed is NLRP3; the disease is age-related macular degeneration.