Recent studies have linked SorL1 to endosomal dysfunction, another pathological feature of AD.[12] Subsequently, two studies on the effect of SorL1 deletion on human induced pluripotent stem cells (iPSCs) were published, both of which demonstrated that SorL1‐deficient neurons undergo significant endosomal enlargement (EE).[13] Pathological EE has been demonstrated in the SorL1 haploinsufficiency minipig model,[14] but the pathology of SorL1 deficiency remains unclear. This evidence concerns the gene SORL1 and Alzheimer disease.