Here, with the goal of testing whether interventional modulation of somatic CAG expansions can be a disease-modifying therapeutic approach to benefit HD-related phenotypes, we used the small molecule naphthyridine-azaquinolone (NA), previously demonstrated to induce en masse contractions of the mutant CAG-expanded allele to less than inherited lengths in brains of HD or DRPLA mice49,50. The gene discussed is ATN1; the disease is Huntington disease.