Accordingly, our results support the hypothesis that increased TSPO expression in the skeletal muscle of SOD1‐G93A is related to increased inflammation mainly mediated by so‐called “protective phenotype,” since the mild stages, and suggest that TSPO may play a role in regulating an anti‐inflammatory and potentially protective macrophage phenotype in the context of ALS along the different disease stages. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.