In the same paper, they demonstrated that also Nuclear Factor κB p65 was higher in ALS spinal cord and inhibition of NF-κB in neurons overexpressing TDP-43 reduces vulnerability to toxic injury [12] suggesting a new pathway of deregulation of TDP-43 in ALS through abnormal activation of NF-κB. The gene discussed is NFKB1; the disease is amyotrophic lateral sclerosis.