Our results suggest as likely that RANTES over-release from Aβ-exposed NAHAs partakes in the multiple proinflammatory effects evoked by Aβ•CaSR signaling and by an Aβ exposure in general, which is in keeping with the views of authors positing that RANTES is a relevant player in the inflammatory cascade that advances AD neurodegeneration [62,104,105]. This evidence concerns the gene CCL5 and Alzheimer disease.