Based on the assumption that cervical cancer is heavily dependent on EGFR activation and on angiogenesis (in turn caused by EGFR activation and HPV infection as well as by the hypoxia-induced VEGF), a phase II trial was designed to compare a multitarget TKI and antivascular agent (pazopanib) and an oral inhibitor of activated HER1 and HER2 (lapatinib). This evidence concerns the gene EGFR and cervical carcinoma.