In the absence of haploinsufficiency mechanisms, this could ameliorate disease phenotypes and has been successfully employed to knock out the mutant rhodopsin (Rho) gene in rodent models of autosomal dominant retinitis pigmentosa (adRP) (Table 1).16,17 As another example, CRISPR-mediated allele-specific knockdown could be extrapolated to treating the autosomal dominant founder mutation (S163R) in the C1QTNF5 gene, which is known to be strongly expressed by the RPE and to cause late-onset retinal degeneration.18 Here, RHO is linked to late-onset retinal degeneration.