To address the contribution of astroglial NF-κB and, more generally, the contribution of astrocytosis to ALS onset and progression, we generated a mouse line expressing an IκBα-DR (IκBαAA) in astrocytes only, under control of the astrocyte-specific glial fibrillary acidic protein (GFAP) promoter, and crossbred them with transgenic mice over-expressing ALS-typical mutant SOD1G93A. The gene discussed is GFAP; the disease is amyotrophic lateral sclerosis.