The loss of the key mCa2+ efflux mediator, NCLX, and decrease in the expression of negative regulators of the mtCU, MICU1 (gatekeeper of mtCU to limit uptake at low iCa2+ and augmenter of uptake at high iCa2+ levels26–29) and MCUB30, is likely to promote increased [mCa2+] levels; especially in the high iCa2+ environment that is reported to occur in neurons during AD progression6. Here, SLC8B1 is linked to Alzheimer disease.