These results allow us to hypothesize that in normal human colon cells, the majority of CpGs in the PIWIL1 promoter are methylated, leading to gene silencing, whereas loss of DNA methylation, which frequently occurs during malignant transformation for delays in maintenance of methylation during accelerated cell division, could in this case drive abnormal PIWIL1 expression in a subgroup of CRCs, as also observed in lung adenocarcinomas [34]. Here, PIWIL1 is linked to lung adenocarcinoma.