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. Studies have found that high-risk HPV can be found in the cervical tissue of almost all cervical cancer patients. Data from epidemiological surveys and laboratory studies have shown 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 the risk of cervical cancer is only present if one is infected with HPV. After human infection with HPV, the viral 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 is cleared by the autoimmune system, i.e. “transient infection”. The other outcome is that the body’s immune system recognizes 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, HPV infection does not necessarily lead to cervical cancer. This is because HPV infection is very common, especially in women of sexually active age. Most HPV infections are cleared by the body’s immune function, so these infections are “transient” and do not cause cervical lesions. Only a few persistent HPV infections cause cervical cancer. It takes a long time, usually about 5 to 10 years, from HPV infection to heterogeneous proliferation of cervical cells and then to invasive cervical cancer. Only high-risk HPV infections cause cervical cancer, while low-risk infections rarely cause cervical cancer. HPV infection is only “viral” and does not necessarily lead to cervical cancer. The detection of HPV infection in clinical tests does not mean that a diagnosis of cervical cancer can be made. The reason is that 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%. In general, 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, and 3.2 times higher for those who have their first birth before the age of 18 than for those who have their first birth at the age of 18. (3) More sexual partners. (4) History of sexual promiscuity or genital viral infections in male partners, etc. (5) Smoking, lack of personal hygiene, chronic inflammatory irritation, viral infections, etc. The right approach to prevent cervical cancer is to insist on regular screening. In the United States, cervical cancer screening is scheduled from about 3 years after a woman starts sexual intercourse, no later than 21 years of age, with termination after 70 years of age; to have more than 3 satisfactory and normal cytology examinations within 10 years. The screening interval is once a year for conventional cytology smears and once every 2 years for TCT, and once every 2-3 years for 3 consecutive normal tests after age 30. Combining HPV screening can reduce the risk of missed cervical cancer.