This suggests that (i) the GLP-1 pathway does not seem to desensitize in response to the Aβ pathology or in general [which is also why GLP-1, but not GIP, analogs were chosen as clinical T2DM treatments (Gault and Holscher, 2018)], (ii) GLP-1 mimetics prevent IR endocytosis through the GLP-1R-mediated suppression of the Ca2+ overload that is provoked by Aβ oligomers and (iii) GLP-1 may prevent the harmful interaction of soluble and extracellular Aβ species with neurons, possibly by promoting insulin-signaling (Bomfim et al., 2012). This evidence concerns the gene INS and type 2 diabetes mellitus.