The commonly accepted pathology of AD involving SorL1 is that SorL1 mediates retrograde transport of APP from the endosome to the TGN, a process that inhibits APP processing into amyloid plaques.[13, 33] Recent studies have shown that SorL1 deficiency causes early endosomes swelling in human induced pluripotent stem cell‐derived neurons (hiPSC‐Ns)[13] and minipig cortical neurons.[14] However, whether the endosome enlargement of SorL1‐deficient hiPSC‐Ns depends solely on the processing of APP into amyloid plaques in the endosome, especially in individuals, is unclear. Here, APP is linked to Alzheimer disease.