Compound heterozygous missense mutations in CCT2 have been identified in individuals suffering from LCA.[2] Computational modeling combined with biochemical studies suggested that these mutations combined induce partial, and not complete, loss of TRiC functionality.[2]CCT2 is a subunit of the eukaryotic TCP-1 ring complex (TRiC, also called chaperonin containing TCP-1 [CCT]); an ATP-driven chaperonin that aids mis- or unfolded proteins in their folding. This evidence concerns the gene MARVELD2 and Leber congenital amaurosis.