Cervical cancer (CC) is a significant public health concern because it remains the fourth most common cancer among women worldwide and the second most prevalent in low-income regions. Even though screening techniques, including HPV DNA testing and Pap smears, have improved with advanced methods and prophylactic HPV vaccines have been introduced, the disease persists due to suboptimal accessibility and uptake in resource-limited settings. Epidemiological studies have associated high-risk human papillomavirus (HPV) infections with more than 90% of cervical cancer cases, as well as other risk factors that include smoking, long-term oral contraceptive use, multiple pregnancies, and even genetic predispositions. Recent studies point out how epigenetic dysregulation played an important part in the pathogenesis of CC. Several mechanisms like DNA methylation, histone modifications, and noncoding RNA-mediated processes play a significant role in aberrant gene expression and tumorigenesis. These insights imply the therapeutic potential of targeting reversible epigenetic alterations, thereby opening promising avenues for new cancer treatments. In this context, this chapter addresses the interface between HPV infection, genetic and epigenetic alterations, and the development of CC, bringing to the fore the urgency to improve preventive strategies and innovative therapeutic interventions.