First, knockdown of EGFR expression by siRNA or blockage of its tyrosin kinase activity using lapatinib (an EGFR inhibitor) inhibited phosphorylation of FAK induced by E2, G1 or OHT in RL95-2 endometrial cancer cells (Figs. 4D and 4E), suggesting that estrogen-induced GPR30 signaling is mediated through EGFR. This evidence concerns the gene GPER1 and endometrial cancer.