Neuroinflammation has emerged as a targetable mechanism in Alzheimer’s disease (AD) over the last ten years, which has been driven by GWAS (Genome Wide Association Studies) signals in several genes (CR1, CLU, TREM2, HLA-DRB5/DRB1, INPP5D, and MEF2C) that are implicated in inflammation [1]. This evidence concerns the gene CLU and Alzheimer disease.