Etiologies that had been reported included structural (e.g., mullerian anomalies), hormonal (e.g., luteal defect), chromosomal (e.g., balanced translocation carriers), immune-related (e.g., anti-phospholipid antibody syndrome), thrombophilias (e.g., factor V Lieden mutations and prothrombin mutations in the caucasian populations), and others. This evidence concerns the gene F2 and thrombophilia.