DCK and cancer: This may be due to fact that: a) the cancer may have an epigenetic/genetic signature that is not predisposed to the induction of terminal differentiation by low dose 5-AZA-CdR; b) the target cancer cells may have a low level of deoxycytidine kinase, the enzyme that activates the prodrug, 5-AZA-CdR [132]; c) the cancer cells may be in anatomic sanctuaries that have low penetration of 5-AZA-CdR (for example, CSF, testis, tumors with a limited blood supply [133]).