We also noted splicing alterations in several channel genes including the transient receptor potential cation channel TRPM4, the sodium channel SCN9A, the chloride channel CLCC1, the voltage-gated potassium channel Kv4.3 gene KCND3, and the voltage-dependent calcium channel CACNA1C. In the case of CACNA1C, the variant made in DM1 cells changes the kinetics and voltage-dependence of inactivation as well as recovery from inactivation [46]. The gene discussed is SCN9A; the disease is myotonic dystrophy type 1.