It is the working hypothesis of our group, that mitochondrial pathology forms the basis of DMD aetiology alongside dystrophin-deficiency [19] (Figure 1), such that much like the damage following eccentric muscle injury (Figure 1A), dystrophin-deficiency-mediated damage could be mitigated if ATP availability was sufficient. The gene discussed is DMD; the disease is hyperinsulinemic hypoglycemia, familial, 4.