HSP90AB1 and Leber congenital amaurosis: The AIPL1 TPR domain alone can interact with Hsp90 in the absence of the FKBP-like domain, and the disruption of the TPR domain by LCA-associated missense mutations, deletions, insertions, duplications, or C-terminal truncations significantly reduced or abolished the interaction with Hsp90 [77,79].