Recent revisions of the amyloid hypothesis of AD, have suggested soluble oligomeric forms of Aβ (oAβ) to be the effectors of Aβ‐induced degeneration, with APOE4 exacerbating oAβ‐associated degeneration relative to other isoforms 41, 42, 70 (Figure 2) (details of participants in Figures 2, 3, 4, 5 found in Table S4). The gene discussed is APOE; the disease is Alzheimer disease.