β‐secretase 2 (BACE2), a homolog of the promising AD therapeutic target BACE1, is poorly understood in terms of expression and functional roles in the CNS.[166] By developing BACE2 loss‐of‐function mutation (BACE2G446R) brain organoids from hPSCs, researchers found that the BACE2 functional mutation led to increased neuronal apoptosis and elevated levels of Aβ oligomers, resembling AD‐associated phenotypes. This evidence concerns the gene BACE2 and Alzheimer disease.