Thus, sodium channel myotonia and paramyotonia congenita are both linked to gain-of-function mutations of the SCN4A gene coding for Nav1.4 sodium channel, while myotonia congenita (MC) is related to loss-of-function mutations in the CLCN1 gene, encoding the chloride channel ClC-1. The gene discussed is CLCN1; the disease is Thomsen and Becker disease.