Taken together, we proposed an interaction network with several hub genes and the indicated regulatory pathways, and suggested that the dysregulation of NF-κB pathway induced by neuroinflammation contributes to the overexpression of fibronectin and a series of fibrotic processes as the major changes in the spinal cord, which could be the potential target for ALS therapy. The gene discussed is NFKB1; the disease is amyotrophic lateral sclerosis.