Rossi et al., using a G93A-SOD1 ALS mouse model showed how the pharmacological stimulation of both CB1 and CB2Rs was able to significantly reduce glutamatergic and GABAergic neurotransmission, and how these receptors were overexpressed in the ALS mice when compared with control animals [77]. This evidence concerns the gene CNR1 and amyotrophic lateral sclerosis.