Objective: Epigenetic mechanisms, including DNA methylation, play important roles in the development of many cancers. The cell cycle inhibitor, p16(INK4a) methylation, has also been linked with cervical neoplasia. However, the relationship between p16(INK4a) methylation and cervical neoplasia is not entirely clear. The aim of this study was to determine the status of p16(INK4a) methylation in cervical neoplasia and to determine the relationship with disease progression or p16(INK4a) protein expression. Methods: Fifty-nine patients, including 21 patients with carcinoma in situ and 31 with invasive squamous cell carcinoma of the uterine cervix, were included in this study. Methylation-specific PCR (MSP) amplification was used to analyze the p16(INK4a) methylation status, while immunohistochemical analysis was carried out to investigate p16(INK4a) expression. Results: MSP analysis revealed that the rate of p16(INK4a) methylation was significantly higher in the cervical neoplasia group than in the control group (55.8% vs. 14.2%, P<0.05). However, we did not establish any correlation between the p16(INK4a) methylation status and the clinicopathologic parameters of cervical cancer, such as clinical stage, tumor size, lymph node metastasis, or parametrial invasion. Furthermore, the immunohistochemistry score for p16(INK4) protein did not correlate with the p16(INK4a) methylation status, diagnosis, and clinicopathologic parameters of cervical cancer. Conclusion: Our data indicate that p16(INK4a) methylation may be used as a good adjunctive test in predicting cervical histology. However, p16(INK4a) methylation status did not predict disease progression or p16(INK4) protein expression.