In previous work, we addressed the role of astrocytic IKK2/NF-κB activation in amyotrophic lateral sclerosis (ALS) pathogenesis using the tetracycline-regulated expression of constitutively active IKK2 (IKK2-CA) under the control of the GFAP promoter (GFAP.tTA/tetO.IKK2-CA) [24,25]. The gene discussed is GFAP; the disease is amyotrophic lateral sclerosis.