It has been previously hypothesized that excreted FGF-2 might act similarly to FGF-1, which readily binds to the FGFR-1 and leads to the spread of reactive astrocytosis, a hallmark of ALS implied in the non-cell autonomous motor neuron death mediated by astrocytes [119]. This evidence concerns the gene FGF2 and amyotrophic lateral sclerosis.