Conditional knockout of EFR3A in the CA3 or CA1 region of the hippocampus in mice inhibits amyloid Aβ-induced presynaptic PIP2 hydrolysis and aberrant neurotransmitter release at the synapse between the Schaffer collateral (SC) and CA1 pyramidal neurons, which ultimately leads to restoration cognitive function and memory in APP/PS1 mice (model for Alzheimer’s disease) [43]. This evidence concerns the gene EFR3A and early-onset autosomal dominant Alzheimer disease.