Taking together with the evidence that cyclin D1 is a direct target of the β-catenin/LEF-1 complex and elevated cyclin D1 expression has been implicated in the pathogenesis of many diseases by stimulating cell proliferation [46, 47], we demonstrated that VDR plays a crucial role in the process of β-catenin entering the nucleus and regulating the transcription of Wnt target genes, VDR levels may contribute to controlling CRC tumour development by inhibiting Wnt/β-catenin signalling, and VDR expression maintenance is closely associated with fewer metastatic CRC diseases in humans. This evidence concerns the gene LEF1 and colorectal carcinoma.