Blocking pro-inflammatory mediators in ALS to reduce neuroinflammation and motor neuron death is a strategy that delayed the onset of symptoms and extended the survival of mutant SOD1 mice (Neymotin et al., 2009; Stommel et al., 2009; Rabinovich-Nikitin et al., 2016); clinical use of a recombinant humanized anti-interleukin-6 receptor (IL-6R) monoclonal antibody is under investigation (Maier et al., 2015; Milligan et al., 2021). This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.