However, neither genetic inhibition of the UPR via ablation of doublestranded RNA-activated protein kinase-like ER kinase (PERK), nor genetic UPR enhancement via ablation of growth arrest and DNA damage-inducible protein 34 (GADD34/PPP1R15A), is beneficial for mutant SOD1-induced motor neuron disease, suggesting that the UPR-PERK pathway is not a likely target for therapeutic intervention in ALS (99). The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.