More importantly, the reduction of BKCa expression using siRNA in Ishikawa cells after E2 treatment could significantly attenuate the expression of p-MEK1/2 and p-ERK1/2 proteins, as well as cell growth and invasion capabilities induced by E2 stimulation, consequently suggesting that BKCa at least partially participates in E2 inducing endometrial adenocarcinoma by activating MEK/ERK pathway. The gene discussed is MAPK3; the disease is endometrium adenocarcinoma.