Riluzole was approved in 1995 and is believed to exert its neuroprotective effects through several mechanisms: (i) Reducing persistent sodium current and firing frequency in ALS neurons back to control levels [30]; (ii) Inhibiting glutamate release and increasing glutamate uptake [142]; (iii) activating various types of potassium channels and inhibiting slow inactivation of voltage-gated potassium channels, thus reducing spontaneous firing and hyperexcitability [143, 144]; and (iv) Inhibiting persistent calcium currents [9, 40, 145] and transient calcium currents [146]. This evidence concerns the gene KCNA3 and amyotrophic lateral sclerosis.