Consistent with these findings, our functional work showed that apical AMD RPE EVs induce disease phenotype in the recipient RPE cells, including prominent ultrastructural changes, such as cytoskeletal disruption, vacuolization, melanin degradation and nucleus malformation, alongside increased protein expression of cytoprotective markers, SOD2 and alpha B crystallin; all features resembling phenotypic alterations in AMD RPE. Here, CRYAB is linked to age-related macular degeneration.