In the amyotrophic lateral sclerosis (ALS) model of mutant SOD1 mice, FGF deficiency causes a significant delay in disease onset, less impaired motor function, and prolonged survival when compared with mice with normal FGF2 levels, probably due to an up-regulation of neurotrophic factors such as CNTF and GDNF [75]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.