Microglia, as the resident macrophages of the central nervous system (CNS), play a vital role as phagocytes and inflammation triggers. The phagocytic capability of microglia is significantly influenced by their activation state, depicted in Figure 1. In neuroinflammation, chronically activated "M1" microglia struggle to efficiently clear damaging proteins, exacerbating tissue damage. Therefore, drugs that can restore normal microglial phagocytosis in a pro-inflammatory environment are promising for neurodegenerative diseases with a neuroinflammatory component. This study demonstrates that human iPSC-derived microglia effectively model altered phagocytic responses induced by various stimuli, providing insights into the potential of new drugs to enhance or restore normal microglial phagocytosis.