However, a study carried out by Camerino et al., showed that ClC-1 chloride channel protein is reduced in patients with SAMS, and this is often associated with alterations of the electromyographic recordings, although patients may have a statin-induced myotoxicity occurring as muscle necrosis due to statin exposure and manifesting with increased CK levels. The gene discussed is CLCN1; the disease is short stature-auditory canal atresia-mandibular hypoplasia-skeletal anomalies syndrome.