TREM2 and Alzheimer disease: Finally, analysis of Ca2+ signaling in human iPSC-derived microglia with genetic deletion of TREM2 (Triggering Receptor Expressed on Myeloid cells 2, a molecule whose rare loss-of-function variants associate with increased risk of AD) revealed higher cytosolic Ca2+ transients in response to ADP, possibly due to a greater release of Ca2+ from the ER and an increased SOCE [135].