In ALS pathophysiology, LPS acts as a potent neuroinflammatory toxin and immunotoxin, stimulating CD14 receptor expressing cells [28] such as monocytes, granulocytes, and macrophages, polarizing the microglia and triggering the release of pro-inflammatory markers such as TNF-α and IL-6. The gene discussed is IL6; the disease is amyotrophic lateral sclerosis.