In our study, RP1-R1933* was infrequent among carriers of EYS-G843E, but this may be attributable to gross differences in the clinical phenotypes considered (macular degeneration or cone-rod dystrophy in the previous reports4,44 vs. canonical ARRP, studied here) Furthermore, while in heterozygous carriers RP1-R1933* seems to exert its pathogenic functions via the co-presence of EYS-G843E and other hypomorphic alleles outside of the RP1 locus4, a reciprocal mechanism is not forcibly true, since molecular pathology of EYS-G843E in ARRP may follow different routes, as clearly shown above. This evidence concerns the gene RP1 and Rod-cone dystrophy.