We found that HPV-positive tumors had significantly higher BCL2 and lower p53 expression than HPV-negative tumors, which is consistent with the hypothesis that the p53 protein inactivated by HR-HPV E6 releases the repression of BCL2 gene which leads to the overexpression of BCL2 protein [41], although it is not clear whether the upregulation of the BCL2 protein is a direct effect of HPV infection or an indirect effect through p53 protein inactivation in breast cancers. This evidence concerns the gene TP53 and breast cancer.