To define whether impaired mCa2+ efflux causally contributes to the progression of AD, NCLX conditional mutant mice (Slc8b1fl/fl, denoted as NCLXfl/fl)22 were crossed with a neuronal-restricted Cre recombinase transgenic model (Camk2a-Cre) to delete NCLX from the forebrain, specifically the prefrontal cortex and CA1 pyramidal cell layer in the hippocampus33. Here, SLC8B1 is linked to Alzheimer disease.