The iQTL, by explicitly identifying APOE ε4 as the interacting factor, provides a possible explanation for the qQTL: if the variant acts primarily in ε4 carriers, and ε4 carriers are enriched at lower expression levels (as both ε4 status and low TMEM106B expression associate with elevated AD risk), then the genetic effect would concentrate at lower quantiles, producing the observed quantile-specific pattern. This evidence concerns the gene APOE and Alzheimer disease.