Recurrent pregnancy loss (RPL) affects approximately 3% of women and is a significant clinical problem. In many cases this phenomenon is associated with thrombophilic complications. An increased risk of thrombophilic complications occurs during pregnancy, owing to reorganization of the coagulation, anti-coagulation and fibrinolytic organisms systems, that are thought to be an evolution adaptation to reduce blood losses in delivery (Kalashnicova 2005). The most common causes of inherited thrombophilias in pregnancy are the Factor V Laden mutation (FV), the MTHFR mutations and mutation in the prothrombin gene G20210A. Caucasians are considered having the higher rate of genetic thrombophilias compared to other racial groups. The prevalence of thrombophilias in women with normal pregnancy outcomes is 2-10% for the FV Leiden mutation, 8-16% for the MTHFR mutations and 2-6% for the prothrombin gene mutation. The only FV mutation is reported in 5% of the healthy white population and 1% of the healthy black population (Ridker 1997). Likewise, in the Asian population these mutations arise at a very low rate in spite of the rate of thrombophilia occurrence is the same as in other populations and is caused by different factors (Thiruchelvam 2009). In the last decade a lot of studies have examined the association of main thrombophilic genes mutations and unexplained RPL in women from different populations. The association of thrombophilic genes polymorphism and RPL is controversial in different studies. Some of these studies have shown an association between thrombophilic genes mutations and RPL (Yenicescu et al., 2009) whereas others have not (Pauer (2003), Hefler (2004)). The objective of this work was to perform a screening of the 3 main thrombophilic genes mutations in Moldavian population, because no such studies have been performed so far, in order to determine the frequencies of these mutations and whether they are associated with RPL. To participate in the study a control group of 100 women with at least 2 normal gestations and no history of abortion and a group of 150 women with RPL were selected. Mutation identification was carried out by specific PCR amplification and restriction analysis. Currently molecular investigations and statistical analysis are pending.