Notably, IFN-γ stimulation enhanced ACSL1 expression in ApoE4-overexpressing HMC3 microglial cells.<h4>Conclusion</h4>These findings provide a new perspective on the involvement of plasma inflammatory markers for AD diagnosis, and suggest a novel link between IFN-γ and APOE ε4-associated AD risk through modulating the ACSL1-driven pathogenic LDAM phenotype. This evidence concerns the gene ACSL1 and Alzheimer disease.