However, the role of NF-κB in different glial cell types is still controversial: NF-κB resulted in the highest-ranked regulator of inflammation in gene array data-sets from astrocytes derived from human post mortem ALS patients [28]; NF-κB was found upregulated in glia and neuronal cells from familial and sporadic ALS patients with TDP-43 (one of the hallmarks of ALS) acting as a co-activator of the p65 subunit of the NF-κB complex [29]. This evidence concerns the gene NFKB1 and amyotrophic lateral sclerosis.