Membrane fluidity, a prerequisite for implantation, is achieved by all the above mediators. The arrival of the zygote in the endometrium is not sufficient to ensure implantation; hormone-dependent changes and the increase in membrane fluidity, also called “receptive endometrium,” are required for successful blastocyst implantation. The establishment of the receptive endometrium to support embryo development and implantation is primarily coordinated by ovarian hormones, progesterone, and estrogen that modulate uterine events. A fine balance of estrogen and progesterone exists in the uterine milieu and has critical role in blastocyst implantation. For instance, implantation requires a preovulatory increase in the secretion of estrogen, which stimulates the proliferation and differentiation of uterine epithelial cells. In the same way, continued production of progesterone by the corpus luteum stimulates the proliferation and differentiation of stromal cells. Even though, both estrogen and progesterone are required for blastocyst implantation, estrogen is a crucial determinant of the window of implantation in mice. McCormack and Greenwald [26] have demonstrated that, in mouse, estrogen plasma level starts to increase from 9th hour, peak at 11th hour on day 4 of pregnancy, and persist for 24 hours [26]. In mouse, blastocyst implantation occurs early morning on day 5 which suggests the critical role of estrogen in blastocyst implantation. It has been previously reported that implantation can be induced in the ovariectomized pregnant mice by single injection of estrogen, which confirms the vital role of estrogen in implantation [27]. The period from 10th to 12th hour on day 4 (time of estrogen peak) appears to be crucial because ovariectomy after these hours does not inhibit implantation [26]. The superoxide anion radical surge at the time of implantation has been implicated for induction of endometrial membrane fluidity (“receptive endometrium”) [1]. An estrogen surge at the time of implantation has been shown to be responsible for a decrease in SOD levels and an increase in superoxide anion radical levels [28].