Studies in rodent models have revealed that HGF administration promotes angiogenic activity, prevents disruption of the blood–brain barrier [20,21,22], and promotes the survival of neurons both after cerebral ischemia [22,23,24,25,26,27] and in a transgenic amyotrophic lateral sclerosis (ALS) model [28,29]. This evidence concerns the gene HGF and amyotrophic lateral sclerosis.