HSPA5 and amyotrophic lateral sclerosis: It is important to remark that this protein interacts with many other cellular proteins and that its dysregulation has been already associated with ALS pathogenesis by mechanisms that a priori do not involve the participation of the CB1 receptor [23,24,25], so the issue will require additional research that may test a cause–effect relationship between dysregulation in BiP function and loss of CB1-mediated neuroprotective effects, and vice versa.