This discrepancy may be due to differences in the increase in microglial number between mice and humans; our data suggest that Spi1/PU.1 may be regulating microglial number, and it is possible that the level of microglial proliferation that can be tolerated by mice and humans is different (particularly given the long course of Alzheimer’s disease in humans). This evidence concerns the gene SPI1 and Alzheimer disease.