ApN could well be a strong alternate candidate for DMD therapy since besides its potent anti-inflammatory properties, it also protects against most common side effects of glucocorticoids such as obesity, hypertension, and glucose intolerance [13], while further improving the myogenic program [18, 49, 50] and upregulating utrophin A. Some novel myokines identified as regulated by ApN in DMD myotubes, like IL-17A or CCL28 may also be additional new targets for the management of this disease. The gene discussed is CCL28; the disease is Glucose intolerance.