In accordance with these observations, we report here that the functional interaction between HPV8E6 and the UV-activated EGFR which we have characterized here has a crucial role in the UV- and HPV8E6-induced skin tumor induction in vivo since the pharmacological inhibition of the RTK-activity of the EGFR suppressed papillomatosis in transgenic mice. The gene discussed is EGFR; the disease is skin neoplasm.