Our present results revealed that treatment with 5-aza-CdR could overcome the SN38-resistance in SN38-resistant subclones established from the ME180 cervical carcinoma cell line, and that neither the methylation status of the DAPK promoter nor the DAPK protein expression level was directly involved in the acquisition of SN38-resistance. The gene discussed is DAPK1; the disease is cervical carcinoma.