Activation of microglial cells in ALS has been extensively characterized and is marked by elevated production of potentially cytotoxic molecules, inflammatory mediators, and proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α) in the toll-like receptor 4 (TLR4) signaling pathway [15, 16]. This evidence concerns the gene TLR4 and amyotrophic lateral sclerosis.