Although the mechanisms underlying the ALS-associated impairment of the neuromuscular unit are still largely undefined, the introduction of positron-emitting tracers targeting the translocator protein 18 kDa (TSPO) permitted the detection of the presence of reactive gliosis and inflammation in the motor cortex of ALS patients [5,6,7,8] and in the brainstem of the SOD1G93A mice as an experimental ALS model [9]. The gene discussed is TSPO; the disease is amyotrophic lateral sclerosis.