Cervical cancer is the second leading cause of female cancer mortalities, worldwide and 5,00,000 new cases are diagnosed annually in developing and developed countries. The epidemiological profile of the disease shows that Cervical cancer is related to sexual activity and associated with Human papillomavirus (HPV) infection.The high risk HPV types 16 and 18 are the most prevelant, representing 69.8% and 15% respectively in cases of invasive cancer. A persistent high-risk HPV infection is also a prerequisite for the development of Cervical cancer. Genomic integration of the viral genome can disrupt several cellular proteins resulting in the upregulation of the tumour suppressor gene P16INK4A which is a cyclindependent kinase inhibitor. Thus over-expression of p16 indicates an already advanced interference of the viral oncoproteins with cellular proteins involved in cell cycle regulation. The protein P16INK4 serves as a surrogate marker for the oncogenic activities of HPV in replication–competent cells of cervical epithelial and its over-expression is well established in Cervical intraepithelial neoplasia(CIN) and Invasive Squamous cell carcinoma(SCC) by many studies.