Human papillomavirus (HPV) is the causative pathogen of over 98% of cervical cancer, which is the second most common cancer in women worldwide. Prior to the development of cancer, HPV establishes persistent infections in the genital tract and successfully evades immune clearance. Members of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) family are important regulators of the innate immune response. HPV proteins can downregulate the expression of STAT1 to allow for stable maintenance of viral episome. STAT5 is another member of this pathway, which plays an important role in controlling cell cycle progression. Several studies reveal that STAT5 is activated in HPV-positive cells and it is necessary for HPV genome amplification. Persistent infection of HPV interacts with abnormal expression of STAT proteins and contributes to the development of cervical cancer. Targeting of these pathways by pharmaceuticals can inhibit HPV infection, which will contribute to the treatment of cervical cancer. The article summarizes the progress on the relationship between HPV and STAT pathway.