In addition, the findings indicate that HIC1 inactivation may function as an initiating event in tumorigenesis based on the propensity of Hic1+/− mice to form spontaneous tumor [24] and the presence of HIC1 silencing events in pre-neoplastic conditions such as smoker's lung, colonic polyps and chronic hepatitis or cirrhosis [14, 15, 17, 25]. This evidence concerns the gene HIC1 and polyp of colon.