Conversely, inhibition of JNK1/2 in HPV- C33A cells had minimal impact on cell growth or colony formation, despite a dose-dependent loss of c-Jun phosphorylation and protein expression (Supplementary Fig. 4A–D), suggesting that HPV+ cervical cancer cells are more sensitive to the effects of JNK1/2 inhibition, corresponding with higher levels of JNK1/2 phosphorylation. This evidence concerns the gene JUN and cervical cancer.