Purpose: To review possible mechanisms of how the fetal semi-allograft avoids immune rejection. Based on these mechanisms potential therapies to improve implantation by suppressing immune rejection are discussed. Materials and Methods: Studies supporting the importance of attaining T suppressor (sup) cells to the maternal fetal interface, while decreasing TH 17 cells along with causing a shift from cellular immunity to humoral immunity by causing a shift of influence from TH1 to TH2 cytokines is presented. Also discussed is the importance of suppressing the ability of natural killer cells to attack the fetal semi-allograft related to the secretion of an immuno-immunomodulatory protein known as the progesterone induced blocking factor (PIBF). Results: Progesterone supplementation in the luteal phase, possibly by causing the production especially of intracellular PIBF, may be the most important therapy to improve embryo implantation by suppressing immune rejection. Other potential therapies include human chorionic gonadotropin (hCG) supplementation and lymphocyte immunotherapy. Conclusions: Knowledge of the mechanism by which the fetal semi-allograft escapes immune surveillance should lead to more novel therapies to improve embryo implantation.