Liao et al., in a study on adult mice with ALS (mSOD1G93A), observed that during the presymptomatic stages of the disease, there was an overexpression of microglia with the M2 phenotype, and as the disease progressed there was a conversion to the M1 phenotype that stimulated the production of prooxidant enzymes, such as nitric oxide synthase (NOX), inducible nitric oxide synthase (iNOs), and cytokine release [39]. The gene discussed is NOS2; the disease is amyotrophic lateral sclerosis.