Our previous study has shown that DDB2 can reduce the abundance of CSCs, which are characterized by enhanced activity of high aldehyde dehydrogenase activity (ALDH+) or CD44+CD117+, in ovarian cancer cell lines, providing a novel mechanism to explain the DDB2-mediated suppression of tumorigenicity, and also suggesting that low expression of DDB2 is essential to maintenance of CSC properties18. This evidence concerns the gene KIT and ovarian carcinoma.