Fibrodysplasia ossificans progressiva (FOP) is a rare disease characterized by extensive bone growth outside of the normal skeleton that pre-empts the body’s normal responses to even minor injuries. It results in what some term a “second skeleton,” which locks up joint movement and could make it hard to breathe. However, new research in mice by a team at the Perelman School of Medicine at the University of Pennsylvania shows that forming extra-skeletal bone might not be the only driver of the disease. Impaired and inefficient muscle tissue regeneration appears to open the door for unwanted bone to form in areas where new muscle should occur after injuries. This discovery opens up the possibility of pursuing new therapies for FOP and was published today in npj Regenerative Medicine.