For example, comparing gene expression profiles of HD mouse models that express exon 1 mutant htt (R6/2) and full-length mutant htt shows no discernable differences between the full-length and fragment models, despite the delayed changes in full-length htt mouse brains, suggesting that N-terminal fragments of mutant htt are the major pathogenic form to induce altered gene transcription [38]. The gene discussed is HTT; the disease is Huntington disease.