This review addresses factors linked to postfertilization phenomena progressing to implantation, particularly as they apply to potential forms of interception. The targets for interception include embryonic development before implantation, tubal transport and tubal milieu, endometrial development before implantation, embryonic signalling to the mother, and embryo-uterine apposition, adhesion, and invasion. Researchers are developing vaccines against zona glycoproteins (ZP2f and ZP3f) to interfere with the preimplantation embryo. They are looking at inactivating strypsin to prevent the hatching of the blastocyst. Researchers are considering targeting the specific binding proteins or glycoproteins expressed during adhesion of the embryo to the uterus to prevent implantation. The endometrial specific proteins IGFBP-1 and alpha2-PEG are other targets for interception. They must be inactivated before implantation to prevent damage to fetal growth. Progesterone deficiency or its impairment of action do not always prevent implantation. Embryos can persist at low levels of progesterone for several days (4-5 days) after they arrive in the uterus. In fact, the embryo's own steroids can maintain a local uterine milieu until it can secrete human chorionic gonadotropin. Failures of interfering with implantation may damage some embryos, cause biochemical pregnancies or blighted ova, and result in pregnancy complications (e.g., placenta previa). Any form of interception must meet high standards of acceptability, efficiency, and safety. We need to better understand the processes of human implantation.