Although the APP, PSEN1, PSEN2, and MAPT genes are considered major pathogenic genes for AD and classic tauopathies [18,19,20], mutations in these genes represent less than 5% of the AD population; consequently, their influence on AD pharmacogenetics associated with conventional anti-dementia drugs is quantitatively negligible; not so in the case of immunotherapy or secretase inhibitors/modulators addressing amyloid-β (Aβ) deposition. The gene discussed is PSEN1; the disease is Alzheimer disease.