Duchenne muscular dystrophy (DMD), caused by mutations in the gene encoding for the cytoskeletal protein dystrophin, is a severe illness characterized by progressive muscle weakness and degeneration. In affected patients this eventually leads to loss of ambulation, respiratory failure, and premature death. In healthy muscle cells, dystrophin interacts with numerous proteins of the so-called dystrophin-associated protein complex (DAPC),1,2 thereby serving as a linker between the cytoskeleton and the extracellular matrix. Disruption of this link in case of dystrophin-deficiency renders muscle tissue vulnerable to mechanical stress.3,4