If we consider that the early stage of ALS is characterised by neuroinflammation exhibiting neuroprotective M2 functions that are lost and converted into M1 toxic actions when disease progression accelerates in SOD1-G93A mice (approximately around 16–18 weeks) [37, 41], the efficacy of the short treatment could be explained by having clemastine sustained neuroinflammation only when it is protective for motor neurons. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.