In cervical cancer, the ubiquitin‐mediated proteolysis pathway can be best characterized by high‐risk HPV‐16 E6 binding activity to the tumor‐suppressor protein p53 to induce ubiquitylation and proteasomal degradation 40, 41, and the abrogation of p53 allows the accumulation of genetic mutations that would normally have been repaired. This evidence concerns the gene TP53 and cervical carcinoma.