Moreover, predictions based on increased CD33 expression and increased plaque burden in human AD brains [99, 100] were not at first glance completely consistent with the outcomes of experiments that reduced CD33 expression in knockout mice and BV2 murine microglia, which resulted in impaired uptake and clearance of Aβ42 in cultured microglia and reduced plaque burden and insoluble Aβ42 in APP/PS1/CD33−/− mice [95]. The gene discussed is CD33; the disease is Alzheimer disease.