There is a study that demonstrated that in the occurrence of dystrophin deficiency, the somatic stem cells are not poised to affect the immediate muscle tissue, yet the overexpression of TEAD1 can ameliorate the pathology by increasing the number of satellite cells [79], and the VGLL3 gene, in combination with the TEAD1 gene, regulates the skeletal muscle myogenesis process [80]. The gene discussed is VGLL3; the disease is hyperinsulinemic hypoglycemia, familial, 4.