We chose to use the SOD1G93A mouse model in these studies, because it demonstrates many key features of ALS, like motor neuron death, inflammation, astroglial and microglial activation, and, relevant to this project, an upregulation of all three UPR sensors IRE1, ATF6 and PERK [53]. The gene discussed is ATF6; the disease is amyotrophic lateral sclerosis.