In Alzheimer disease (AD), in which the role of different HSPBs was analyzed, it was demonstrated that HSPB8, HSPB6, and HSPB2 co-localize with cerebral amyloid angiopathy (CAA) in AD brains; notably, in human leptomeningeal smooth muscle cells and human brain astrocytes, HSPB8 increases the secretion of the inflammatory factors interleukin-8 (IL-8), soluble ICAM-1, and monocyte chemoattractant protein 1, suggesting that HSPB8, possibly working in conjunction with other HSPBs, can act as a mediator of the inflammatory reactions associated with CAA [82]. This evidence concerns the gene HSPB8 and cerebral amyloid angiopathy.