Indeed, there is growing evidence that increased mRNA and protein level account for 2.5% and 55% in human colorectal cancer, respectively, which indicates that the upregulated cyclin D1 protein level does not occur solely as a consequence of gene amplification [16] and the defective post-translational regulation such as the proteasomal degradation may result in the upregulation of cyclin D1 protein level [34, 35]. Here, CCND1 is linked to colorectal cancer.