Existing evidence suggests that HPV16 may synergize with HIF-1α to promote malignancy, while E6/E7 proteins impede keratinocyte differentiation [51, 52] Differences in viral tropism and oncogenic potential further underscore the intertwined biology of HPV and histology in cervical cancer, supporting the integrated subtyping approach employed in this study. This evidence concerns the gene HIF1A and cervical carcinoma.