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