Our findings here confirm these original findings in additional FAP colon biospecimens and extend our current mechanistic understanding of the role of ETHE1 in FAP CRC tumorigenesis with both in vitro and in vivo studies, leading to the following salient conclusions: First, because ETHE1 promotes CRC cell growth, and is upregulated in phenotypically normal APC+/- FAP colon epithelium, high ETHE1 levels may be useful as an early biomarker of CRC premalignant risk. This evidence concerns the gene FAP and colorectal carcinoma.