ATP5F1E and Duchenne muscular dystrophy: On the other hand, and at variance from mitochondria of normal donor (Fig. 5A,B—a part), upon the addition of the F0F1 ATPase inhibitor oligomycin mitochondria of DMD patients readily depolarized after the expected hyperpolarization (Fig. 5A,B—b and c parts), suggesting a latent dysfunction (e.g., Ca2+ deregulation; Angelin et al., 2008) that can be unmasked by inhibition of the ATP synthase.