Blockage of proinflammatory mediators (e.g., IL-6, IL-1, TNF-α, COX-2, and CXCR4) in ALS to modulate neuroinflammation and decrease MN death is another strategy that resulted in delayed symptom onset and prolonged survival of mSOD1 mice, and clinical trials for these compounds are ongoing (4, 123, 126–134) (Table 1). The gene discussed is IL1B; the disease is amyotrophic lateral sclerosis.