We note that genetic variants from frequently associated loci tended to produce the most consistent AD‐relevant phenotypes (eg, SORL1, ABCA7, PLCG2), although many of the more exploratory variants also generated AD‐like expression signatures across multiple modules in aging mice (eg, CEACAM1, MTMR4) (Figure 2). This evidence concerns the gene SORL1 and Alzheimer disease.