These include, for example, pharmacological treatments (e.g., glucocorticoids, angiotensin-converting enzyme [ACE] inhibitors, and β-blockers), genetic modifiers associated with dystrophin deficiency and muscle degeneration (e.g., latent TGFβ binding proteins [LTBPs] and the ACTN3 gene encoding α-actinin-3), and DMD mutations [8, 10, 11]. The gene discussed is ACE; the disease is neuromuscular disease caused by qualitative or quantitative defects of dystrophin.