This could include developing a PMS1-specific splice modulator for pseudo-exon inclusion.37 Knockout of either Msh3 or Pms1 in mHtt CAG 140 knock-in mice has recently been shown to alleviate molecular phenotypes in Huntington’s disease–vulnerable striatal neurons (e.g. lack of mHTT aggregates at 6 months),38 further illustrating potential therapeutic relevance. The gene discussed is PMS1; the disease is Huntington disease.