SorL1 mediates the intracellular sorting of APP, including retrograde transport from endosomes to the TGN, as well as the transport of Aβ from endosomes to lysosomes.[7] These sorting routes are critical for inhibiting the processing of APP to Aβ, the neurotoxic hallmark of AD.[31] We measured the abundance of full‐length APP in the SorL1 KO hippocampus and found that it was elevated by 36.9% (Figure 1E,G), indicating that the intrinsic disturbance of APP processing was caused by SorL1 depletion. This evidence concerns the gene APP and Alzheimer disease.