In 2007, haplotype insufficiency of Sortilin‐related receptor 1 (SorL1) was found to increase the risk of Alzheimer's disease (AD).[1] Exome sequencing revealed that SorL1 coding variants are closely associated with early‐onset familial AD.[2] Mutations with coding sequence truncation occurred exclusively in AD patients,[2, 3] confirming the role of SorL1 as a critical protector against AD. This evidence concerns the gene SORL1 and early-onset autosomal dominant Alzheimer disease.