Based on this evidence and on the fact that the restoration of NO signalling by nNOS overexpression ameliorates muscle function [14,15], genetic and pharmacologic strategies to boost nNOS/NO signalling in dystrophic muscle are being tested with encouraging results: in particular, the combination of NO donation with non steroidal anti-inflammatory activity limits muscle damage and favours muscle healing in vivo [16-18] such that it is currently being tested as a therapeutic for Duchenne muscular dystrophy in humans [19,20]. Here, NOS1 is linked to Duchenne muscular dystrophy.