SPI1 and amyloidosis: Byungwook Kim et al. reported a significant increase in soluble amyloid-β (Aβ) levels, amyloid plaque deposition, and microglial formation upon downregulation of SPI1; conversely, overexpression significantly improved these phenotypes and nutritional deficiency in neuronal processes.34 Overexpression also increased resistance to apoptosis in microglia, whereas knockdown increased susceptibility.35 These studies indicate that the role of SPI1 in regulating the cell cycle varies across different cell types and diseases.