It has been reported that melatonin not only effectively delays the progression and mortality of the disease but also significantly inhibits motor neuron death by inactivating the receptor interacting protein-2 (Rip2)/caspase-1 pathway and caspase-3 and blocking the release of mitochondrial cytochrome c in a mutant superoxide dismutase 1 (SOD1) (G93A) transgenic mouse model of ALS [141]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.