In our results, WNT4 and JIP2 dramatically rescued the role of E6 in promoting cancer cell proliferation both in vitro (Fig. 3b, e, f) and in vivo (Fig. 4a–e), suggesting that the β-catenin-independent, noncanonical WNT/PCP/JNK pathway, especially WNT4 and JIP2, could be an ideal target for treating HPV-induced cervical cancer. The gene discussed is WNT4; the disease is cancer.