This result led us to hypothesize that in AD model, the full‐length APP mostly produces Aβ through the β, γ‐secretase‐mediated cleavage pathway, while the full‐length APP level located on the PM is relatively low, but our experimental data indicate that the levels of full‐length APP located on the PM are significantly upregulated in APP/PS1 mice stimulated by 40 Hz light flicker, increasing its interaction with KCC2, which is likely to be involved in the post‐translational modification process of KCC2. The gene discussed is SLC12A5; the disease is Alzheimer disease.