More recently, genome-wide association studies have implicated CALM variants in Alzheimer’s disease [13], which again may be related to changes in the localisation of SNAREs, because even slight perturbations in the trafficking of the Amyloid Precursor Protein, its binding partners (e.g., SorLA), and/or its proteases can all lead to increases in the production of amyloidogenic peptides [14]. This evidence concerns the gene SNAP91 and Alzheimer disease.