The current view is that in cervical cancer c-fos/c-jun heterodimer formation results from the inefficient expression of the ternary complex factor Net [25], but the evidence we have uncovered for HPV16E6 dependent c-fos expression after H2O2 or TGF-α stimulation broadens the scope of the mechanisms of c-fos/c-jun heterodimer formation in extracellular conditions such as oxidative stress. The gene discussed is JUN; the disease is cervical carcinoma.