This phenotypic variability could be explained by the presence of additional genetic modifier variants other than the RP1 gene, or the presence of a variant within the non-coding regions in RP1. Furthermore, as in Bardet–Biedl syndrome [60], the pathomechanism could show oligogenicity, in which two or more recessive genes variants may lead to IRD phenotypes when the variants act together [61]. The gene discussed is RP1; the disease is Bardet-Biedl syndrome.