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with a history of muscle cramps in the legs was observed in one of 3 patients with *MGAM* c.3202G \> A (Fig. [3](#Fig3){ref-type=”fig”}b). The patients with *MYH7* c.1506A \> G or *MYBPC3* c.2695G \> A (Fig. [3](#Fig3){ref-type=”fig”}c, d, respectively) are common genetic cause of childhood onset of HCM. Clinically these 2 patients are presented with left ventricular outflow tract obstruction in addition to classical HCM features.Fig. 3Characterization of glycogen storage myopathy (GSM). **a** Fiber with lysosomal glycogen storage in the muscle biopsy of a patient with GSM (consistent with glycogenosis type 1). **b** Sequence alignment of *MGAM* c.3202G \> A mutation (red box) with the human wild type and other homologues. **c**-**d** CT myocardial slices of patients with *MYH7* c.1506A \> G (**c**) and *MYBPC3* c.2695G \> A (**d**) mutations showing mid-myocardial hyper-enhancement and a large area of delayed hyperenhancement (green arrows). **e** Sequencing chromatograms of *SGCB* c.1588G \> A mutation (red box) and the wild type. **f**-**g** A reduction of glycosylation of gC1qR (**f**) and an increase in molecular weight of CKMM (**g**) in muscle biopsy of a patient with *SGCB* c.1588G \> A mutation. The molecular weight of gC1qR is shifted to a higher molecular weight bands due to the presence of glycosylation. **h**-**i** Multiple muscle magnetic resonance imaging of a patient with *SGCB* c.1588G \> A mutation showing increased T1 relaxation time in the medial left
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