3). These results were supported by earlier reports that over-expression of EGFR in prostate and ovarian cancer was associated with activation of the PI3K/AKT signaling pathway [22,23]. Moreover, treatment of EGFR inhibitor abolished p53-R175H-induced cell invasion and migration and attenuated activation of AKT (Figure. 4), suggesting GOF effects of this mutant could drive invasive characteristics in EC cells through EGFR/PI3K/AKT-dependent pathway. This evidence concerns the gene TP53 and ovarian cancer.