The finding of the heterozygous missense variant NM_000257.4(MYH7):c.1499A > C (p.Glu500Ala) in a single patient with HCM, but not skeletal myopathy (Table 1) [13, 25], may indicate that loss of a negative charge at that particular site disrupts these salt bridges, thereby inducing structural changes that ultimately lead to a net increase in myocyte contractility, a feature found in HCM. The gene discussed is MYH7; the disease is skeletal muscle disorder.