As we’ve shown in this review, the relationship between each of these parameters and PPARγ MOA is empirically justified, and we recommend that future large-scale AD drug trials of PPARγ agonists or of the PPARγ/δ dual agonist T3D-959, incorporate measurements of fasting insulin, Aβ peptides and p-tau 181 as covariates. This evidence concerns the gene INS and Alzheimer disease.