This seems quite clear in the handful of cases wherein the carrier of a high-penetrance FAD mutation has been spared from dementia—as well as glucose aberrations, tau pathology, and cerebral atrophy—by a genetic variation in the apolipoprotein E gene (APOE) pathway, despite very high accumulation of Aβ (Raulin et al., 2022; Troutwine et al., 2022). The gene discussed is APOE; the disease is Cerebral atrophy.