As we have shown that distinct GCs have different abilities to modulate FAP differentiation and that their effect is dependent on whether the target cells are actively growing or have reached confluence and stopped cycling, it is difficult to predict how GCs that are currently used to treat muscular dystrophies are impinging on FAP plasticity while these progenitor cells cycle between the proliferative and resting state that characterize DMD. Here, FAP is linked to muscular dystrophy.