Cervical cancer is the only cancer with a clear cause among all human cancers to date. The “culprit” of cervical cancer is a virus called human papilloma (HPV). Studies have found that high-risk HPV can be found in the cervical tissue of almost all patients with cervical cancer. Data from both epidemiological surveys and laboratory studies indicate that HPV infection is a major prevalent factor in cervical cancer. It can be said with certainty that HPV infection is a necessary prerequisite for the development of cervical cancer, and that only infection with HPV puts one at risk of developing cervical cancer. After the human body is infected with HPV, the virus gene can be integrated into the epithelial cells of the cervix, and two types of regression may occur: for people with normal immune function, the duration of infection is relatively short, usually around 8-10 months, and the virus will be cleared by the autoimmune system, which is a “transient infection”. The other outcome is that the body’s immune system can recognize the HPV infection but is unable to clear it, resulting in the persistence of the infection, which in turn causes proliferation, heterotypic changes in the cervical cells, and eventually cancer. However, infection with HPV does not necessarily lead to cervical cancer. This is because: (1) HPV infection is very common, especially in women in the sexually active age group. (2) Most HPV infections can be cleared by the body’s immune function, so these infections are “transient” and do not cause cervical lesions. (3) Only a few persistent HPV infections cause cervical cancer. (4) It takes a long time from HPV infection to heterogeneous proliferation of cervical cells to invasive cervical cancer, usually about 5 to 10 years. (5) Only high-risk HPV infections cause cervical cancer, while low-risk infections rarely cause cervical cancer. (6) HPV infection is only “viral” and cannot be said to necessarily cause cervical cancer. The detection of HPV infection in clinical tests does not mean that cervical cancer can be diagnosed. It is because HPV needs to go through a series of transformation processes to develop normal cervical cells into cervical cancer. Cervical intraepithelial neoplasia (CIN) is usually used to reflect the evolution and progression of cervical cancer, which includes cervical atypical hyperplasia and cervical carcinoma in situ, while cervical atypical hyperplasia is commonly referred to as cervical “precancerous lesions”. The overall risk of developing invasive cervical cancer from cervical intraepithelial neoplasia is 15%. Generally speaking, the higher the level of cervical intraepithelial neoplasia at the time of detection, the higher the risk of developing cervical cancer. Therefore, early diagnosis and treatment are essential to improve the outcome of cervical cancer treatment. Any woman with a history of sexual intercourse is inevitably at risk for HPV infection. Therefore, the initial detection of HPV infection should not be overly stressful. However, this does not mean that HPV infection can be taken lightly because the risk of cervical cancer increases significantly with persistent or recurrent infection, or even with simultaneous infection with different types of the virus. Risk factors for persistent HPV infection and precancerous cervical lesions include: (1) Early age of sexual initiation, early childbearing, and multiple births. (2) The prevalence of cervical cancer is 13.3-25 times higher for those who have their first sexual intercourse before the age of 18 than for those who have their first birth after the age of 20; 3.2 times higher for those who have their first birth before the age of 18 than for those who have their first birth after the age of 18. (3) More sexual partners. (4) History of sexual promiscuity or concurrent genital viral infections in male partners, etc. (5) Smoking, inattention to personal hygiene, chronic inflammatory stimulation, viral infection, etc. To prevent cervical cancer, the right approach is to insist on regular screening. In the United States, cervical cancer screening is scheduled from about 3 years after a woman starts her sexual life, no later than 21 years old, and terminates after 70 years old; to have more than 3 satisfactory and normal cytological examinations within 10 years. The screening interval is once a year for conventional cytology smear; once every two years for cervical fluid-based thin-layer cytology (TCT); and once every 2-3 years for those who have 3 consecutive normal examinations after the age of 30. The 2004 guideline recommendation of the China Cancer Research Foundation for cervical cancer screening suggests that the starting time of screening is 25-30 years old in economically developed areas and 35-40 years old in less economically developed areas, and all high-risk groups should be appropriately advanced. The termination time is set at 65 years of age. The interval is once a year, with two consecutive normal intervals extended to 3 years; 2 consecutive negative HPV intervals can be extended to 5-8 years.