UTRN and neuromuscular disease caused by qualitative or quantitative defects of dystrophin: A better comprehension of the molecular and cellular processes that underlie the sparing of extraocular muscles during the course of disease progression in dystrophinopathy could be helpful for the identification of new therapeutic targets to counteract dystrophin deficiency, i.e. manipulation of calcium handling, utrophin replacement therapy, the targeted upregulation of molecular chaperones or improving the capacity for cellular regeneration.