Remarkably, a similar mechanism has been proposed for an RP-mutant form of PRPF31 that is thought to sequester its interactor PRPF6 out of the tri-snRNP [31], and an altered composition of the tri-snRNP has also been described for RP-causing missense mutations in PRPF8 [21]. This evidence concerns the gene PRPF8 and retinitis pigmentosa 1.