For example, the fact that VAPB-3 shares similar properties with P56S-MSP as regards membrane interactions, means that even without carrying any ALS-causative mutation, a person might develop ALS through a mechanism underlying ALS8, if VAPB slicing variants like VAPB-3 get accumulated in cells to a certain degree, due to proteasomal inhibition triggered by pathological and/or environmental conditions. This evidence concerns the gene VAPB and amyotrophic lateral sclerosis.