The consistent > 2-fold increase in affected D2 and SJ recombinants, suggests Dysf (or another SJ variant, or SJ pathology in common with A/J) and lack of C5 (or other D2 change in common with A/J) may also have unknown modifying roles in susceptibility to EM/HD and could help explain the remaining missing heritability. This evidence concerns the gene DYSF and Huntington disease.