While it is hypothesized that changes to channel gene expression underlie many of the physiological abnormalities reported in mouse models of HD, it is clear that the deletion of the N17 domain results in changes to gene expression in BACHD mice [48], the Q31 (BACWTΔN17) model may also experience changes at the genomic level and future studies of this model may be useful in understanding how the various domains of the Htt gene influence transcription. Here, HTT is linked to Huntington disease.