Emerging research elucidates metabolic pathways influencing neuroinflammatory conditions. A study published in Nature Metabolism uncovered cholesterol metabolism’s central role in sustaining chronic neuroinflammation by microglia after stroke, hindering recovery. Additionally, activation of the lipid-driven LC3-associated phagocytosis (LAP) pathway has been demonstrated as critical for immune function. In HIV infection, the Tat protein impairs macrophage autophagy, promoting tuberculosis co-infection by disrupting cellular cleaning mechanisms. These mechanistic insights provide novel targets for therapeutic intervention against neuroinflammatory and infectious diseases.