Besides the disturbances observed in the expression of CRT and CRMP4a, other components of the Fas/NO pathway, such as p38 kinase, ASK1, or neuronal nitric oxide synthase, were shown to be activated or increased in the spinal cord of ALS mouse models starting at presymptomatic stages of the disease [27, 33–40]. The gene discussed is FAS; the disease is amyotrophic lateral sclerosis.