More specifically, studies performed using mice modeling DM1, HD, spinocerebellar ataxia type 7 and spinocerebellar ataxia type 1 indicate that the chromatin, transcription and replication status at repeats modulates repeat instability through gene-specific cis-elements, which include CCCTC-binding factor (CTCF) sites, CpG islands and replication origins [26,27,28,29]. Here, CTCF is linked to Huntington disease.