The interaction of active GLP-1R with VAPB was deemed functionally relevant, as it was no longer present when VAPB P56S, a self-aggregating loss-of-function VAPB mutant associated with amyotrophic lateral sclerosis (ALS)16,17, was expressed instead of its wildtype (WT) counterpart (Supplementary Fig. 1g–i), and as both VAPB knockdown by RNAi (Fig. 1k and Supplementary Fig. 1j, k), and overexpression of VAPB P56S, but not of WT VAPB (Supplementary Fig. 1l), significantly reduced the capacity of GLP-1R to potentiate insulin secretion from INS-1 832/3 cells. This evidence concerns the gene INS and amyotrophic lateral sclerosis.