This study, combined with the anti-inflammatory, antioxidant, antiapoptotic, and immunological effects on the CNS reported in the literature, encouraged Ratan et al. [119] to evaluate the effects of the ginsenoside Re (G-Re) (59) (Figure 8) on neuroinflammation and its action on human superoxide dismutase 1 (SOD1) through the administration of 2.5 μg/g of the compound in symptomatic ALS hSOD1G93A mice. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.