In cervical cancer, a number of experimental studies have consistently shown that although numerous events drive the malignant conversion of cervical carcinoma cells, E6/E7 expression appears to be continuously required to maintain their malignant phenotype [36-38]; in fact, removing E6 and E7 proteins from HeLa cells via a recombinant virus that expresses the bovine papillomavirus E2 protein led to growth inhibition and impaired activation of p53 and Rb pathways and repression of E2F-responsive genes inducing growth inhibitory signals to the cells [39]. Here, TP53 is linked to cervical cancer.