Our results, however, pinpoint to an increased likelihood of causality because (1) they were reproduced in two independent populations, including different ethnicities, which offer a natural means of effect randomization (hence, minimizing the influence of confounders), (2) they showed a dose-response (TAPBP hypomethylation was associated with increased survival relative to hypermethylation), and (3) they yielded a cancer driver potential for TAPBP that was comparable to that of known cancer driver genes. Here, TAPBP is linked to cancer.