In the current study, an antibody with greater selectivity for toxic AβO was generated to maximize efficacy against AD by reducing unproductive binding to the more abundant non-toxic Aβ species (monomers, large/HMW soluble aggregates, insoluble fibrils/plaques) and increase safety by preserving normal Aβ function and decreasing the risk of adverse effects (ARIA) associated with the engagement of plaque and vascular deposits18–20. The gene discussed is ABO; the disease is Alzheimer disease.