DLG4 and fragile X syndrome: Others have shown that hexanucleotide expansions in a non-coding region of C9orf72 enable the formation of G-quadruplexes in both the genomic DNA and transcript RNA that result in abortive transcription and the development of neurodegenerative disease pathologies.[6] Also, G-quadruplex formation in the untranslated region of Post-synaptic density protein 95 (PSD-95), which is prone to trinucleotide-repeat expansion and pathogenic for Fragile X syndrome, regulates access of miR-125a and modulates translation of PSD-95 mRNA [7].