The hypothesis derived from both paradigms is that the neuroprotective effects associated with the activation of the CB1 receptor in experimental ALS [18,19,20], as well as those described in experimental PD [15,16,17], could be related to a modulation of CB1 receptor function by BiP, which would be conceivable for their recently-demonstrated physical interaction [22], but this will be the objective of future work. Here, HSPA5 is linked to amyotrophic lateral sclerosis.