Shared repeat expansion disorder modifier mechanisms were initially suggested through an analysis of Huntington’s disease and polyglutamine spinocerebellar ataxias, where variants in FAN1, PMS2 and RRM2B displayed significant associations.21 In our work, we assessed recent data from an XDP-modifier GWAS, a study highlighting the importance of MSH3 and PMS2. Here, MSH3 is linked to juvenile Huntington disease.