Additional motivation came from the observations that: 1) an 83 amino acid deletion at the N2A-PEVK intersection in muscular dystrophy with myositis (mdm) mice leads to early muscle degeneration and death22; and 2) the mdm mutation prevents the increase in titin stiffness that normally occurs upon activation of wild type muscles, perhaps by disrupting titin-actin interactions23. This evidence concerns the gene TTN and myositis disease.