After using antibodies against TLR2/4 or CD14, or alternatively blocking this pathway by using CD14-/- microglia, it was found not only the decreased production of pro-inflammatory cytokines and free radicals but also the increased release of IGF-1 from mSOD1G93A microglia, thereby weakening neurotoxicity and enhancing the neuroprotective effect of microglia, which indicates that activation of microglia through the CD14 and TLR pathways is one of the neuropathological markers of ALS. This evidence concerns the gene CD14 and amyotrophic lateral sclerosis.