In addition, the muscle atrophy observed in DMD patients is not the consequence of an activation of the myostatin pathway nor to an overexpression of ACTIVIN A. On the contrary, our data indicate that the myostatin pathway, including ACTIVIN A expression, may be intrinsically down-regulated in atrophying or wasting muscle diseases to counterbalance the wasting process. Here, MSTN is linked to Duchenne muscular dystrophy.