However, the fact that mutant SOD1 mice with a constitutive depletion of TNFR1 have a shorter lifespan suggests that the activity of this receptor in the various cell types may be balanced during ALS course, possibly depending on the levels of TNFα and/or on the activity of the antithetic TNFR2 receptors in the same cells. This evidence concerns the gene TNF and amyotrophic lateral sclerosis.