In these cases, the participation of proinflammatory cytokines have been demonstrated [71], alike amyotrophic lateral sclerosis, in which IFNγ contributes to the cross-talk between motoneurons and astrocytes, and has been proposed to contribute to motoneuron death by eliciting the activation of the lymphotoxin-β receptor (LT βR) through its ligand LIGHT [72,73]. The gene discussed is LTBR; the disease is amyotrophic lateral sclerosis.