We chose to study EphB2, EphA4 and E‐cadherin processing based on their documented function and important signalling in different physiological and pathophysiological contexts, such as synaptic plasticity, memory formation, cell proliferation and cancer,27, 28, 29, 30, 31, 32, 33 which have been implicated in the adverse events associated with γ‐secretase inhibitor trials in AD patients.13, 14. The gene discussed is EPHB2; the disease is Alzheimer disease.