Our general objective in this study was to investigate the consequences of a heterozygous deficiency of the BiP protein, which, by potentially acting as an interacting protein, has been recently associated with CB1 receptor function [22], in two neurodegenerative disorders in which the activation of this receptor is known to be neuroprotective: ALS [18,19,20] and PD [15,16,17]. This evidence concerns the gene HSPA5 and amyotrophic lateral sclerosis.