This relationship is evident in ALS, where astrocytes secrete toxic soluble factors including proinflammatory signaling molecules TNF-α [34], TGF-β, IL-6, IFN-γ, and nitric oxide [35] and overexpress the astrocytic proinflammatory marker C3 in human spinal cord and motor cortex, which has been correlated with the onset of ALS-associated symptoms in the SOD1G93A mouse model of ALS [36]. The gene discussed is IFNG; the disease is amyotrophic lateral sclerosis.