HPV is a well‐established driver of cervical cancer, aiding tumor persistence.[71] High‐risk HPV types, particularly HPV16 and 18, contribute to most cervical lesions.[9] The HPV genome regulates viral replication and progression, often integrating into host chromosomes and promoting carcinogenesis via viral oncoproteins.[8, 72] These oncoproteins activate signaling pathways, including STAT3/NF‐κB, thereby inducing immune suppression and facilitating tumor immune evasion.[73, 74] In our study, HPV16 was detected in 72.9% of patients, coinciding with higher STAT3 and SNAIL expression. Here, SNAI1 is linked to neoplasm.