Almost all CRC patients had abnormal β-catenin signal transduction pathway[26] and 25(OH)D in colon and several other tissues could be converted into hormonally active 1,25(OH)2D3 which could inhibit the abnormal signal pathway, and promote the differentiation of tumor cells by stimulating β-catenin-TCF-4 target gene [27, 28] and inducing E-cadherin [29, 30]. This evidence concerns the gene CDH1 and colorectal carcinoma.