MSH3 and Huntington disease: Nevertheless, although our data clearly show the lack of modification of HD onset by CAG repeat size polymorphisms in other polyglutamine disease genes, they do point, along with the complex coding hexamer repeat in TCERG176 and a complex nonamer coding repeat in MSH3,21 to the potential of finer delineation of other tandem repeats across the genome as a potential source of modifiers that could further refine the HD landscape and inform the development of treatments for HD.