We devised a straightforward two-factorial experiment employing the colorectal cancer cell line, RKO, in which the molecular mechanisms following 5-AZA-CdR treatment have been well characterised.43 We treated RKO cells with a wide range of AZA concentrations (100−1250 nM) that we envisaged would flank the range of reported in vivo dosages.44 The cells were quickly washed with buffer containing the cytidine deaminase inhibitor tetrahydrouridine45, 46 to dampen any deamination of AZA during the subsequent processing steps. This evidence concerns the gene CDA and colorectal cancer.