Increased O2•− and H2O2 production activates Toll-like receptor 2 (TLR2) and TLR4 signal transduction through IL-1 receptor-associated kinase (IRAK), BH3 domain-only, tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6), and the IκBα-p50/p65 pathway, eventually increasing the proinflammatory cytokine expression characteristic of ALS (174) (Fig. 5C). This evidence concerns the gene TRAF6 and amyotrophic lateral sclerosis.