Not only a shift towards factors promoting M1 phenotype (tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-18, IL-6, and endothelial nitric oxide synthase (iNOS)) can be observed in ALS mouse models and patients but also the respective signaling pathways (nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated kinases 1 and 2 (ERK1/2), and Signal transducer and activator of transcription 3 (STAT3)) seem to be affected in ALS [11–19]. Here, STAT3 is linked to amyotrophic lateral sclerosis.