The results of this study of gemcitabine resistance in cervical cancer cells and its reversion with the weak DNA demethylating agent hydralazine show that the development of resistance is accompanied by down-regulation of key genes for gemcitabine's intracellular uptake and metabolism, hENT1 and dCK. Interestingly, this down-regulation was not due to gene promoter hypermethylation as demonstrated by MSP and bisulfite sequencing; nevertheless, hydralazine was able to reactivate their expression and to revert gemcitabine resistance. Here, DCK is linked to cervical carcinoma.