It is noteworthy that LCA is mainly recognized as a disease of the retinal pigment epithelium and photoreceptors[14] and only two sibling patients with variants in CCT2 resulting in disruption of TRiC were implicated in LCA to date.[2] Variants in CCT5 have not been associated with patients suffering from LCA as yet, making further studies necessary to fully understand the consequences of impaired F-actin filament formation for LCA. The gene discussed is MARVELD2; the disease is Leber congenital amaurosis.