Flk-1 overexpression in spinal motoneurons of the ALS SOD1 mouse model (with mutations in the gene encoding the antioxidant copper/zinc superoxide dismutase) has been shown to delay both neurodegeneration and disease onset [67], being the primary mediator of the neuroprotective and anti-excitotoxic effects of VEGF on motoneurons [37,38,68]. This evidence concerns the gene KDR and amyotrophic lateral sclerosis.