On account of the fact that ChemR23 might be indeed expressed on astrocytes and it bears a protective role, a recent study performed a chronic and peripheral treatment with RvE1 and LXA4 alone or in combination in a mouse model of Alzheimer’s disease and found that the combined treatment potently reduced astrocyte activation in both hippocampus and cortex and ameliorated AD pathology and the production of several cytokines and chemokines (Kantarci et al., 2018). This evidence concerns the gene CMKLR1 and Alzheimer disease.