It has been well established that E6 and E7 are able to respectively degrade and inactivate the tumor suppressors p53 and pRb, leading to deregulated cell cycle progression without the induction of cell apoptosis and senescence.3,4 In addition to p53-dependent mechanisms, E6 has been shown to stimulate more cancer-causing changes, including enhanced telomerase activity, tumor suppressor protein degradation, such as Scribble and Dlg, oncogenic miRNA regulation, and WNT signaling augmentation.5–8. The gene discussed is TP53; the disease is cancer.