Taking into account that LCLs are easier to manipulate and culture than genetically engineered neurons or pluripotent stem cells, while faithfully recapitulating epigenomic signatures (Hadar et al. 2016) and providing material for multiple experiments, we tested the effect of AD-associated AKAP9 missense mutations on Tau and Aβ using 28 LCLs from AD cases and controls with or without the rs144662445 and rs149979685 variants. This evidence concerns the gene AKAP9 and Alzheimer disease.