Our result is consistent with the recognized link between impaired reduction-oxidation status and the development of HTN [19]–[21], and the observed protective effects in vanin-1−/− mice in a variety of diseases, including oxidative stress [26], intestinal inflammation [27], and colon cancer [28], mostly due to higher glutathione storage to maintain a more reducing environment. This evidence concerns the gene VNN1 and malignant colon neoplasm.