Understanding the phenotypic impact of CD33 LOF may inform on-going industry efforts to antagonize or genetically delete CD33 for Alzheimer’s disease [11] as well as various cell therapies for the treatment of hematological cancers in which CD33 is either genetically deleted as a mechanism to improve therapeutic cell selection and engraftment or CD33 itself is an effector target of the cell therapy [12–15]. The gene discussed is CD33; the disease is early-onset autosomal dominant Alzheimer disease.