On the other hand, though alteration of NF-κB-signalling has been widely linked to ALS onset and progression, [15], [17], [23], [24], our results suggest that, upon chronic inhibition of the NF-κkB pathway specifically in astrocytes, compensatory effects occur in double transgenic mice where the toxic activity of mutant SOD1 is still present. The gene discussed is NFKB1; the disease is amyotrophic lateral sclerosis.