Abstract 373 We generated a mouse model of thrombophilia by combining two common risk factors for thrombosis in humans; transgenic for high levels of FIX (TgFIX+) and activated protein C resistance due to factor V Leiden mutation (FVLQ). Breedings were used in which both parents were heterozygous for the FVL (FVLR/Q) mutation, but only one carried the TgFIX+(resulting in ∼5-fold higher of normal levels). More than 200 newborns were obtained but surprisingly no animal of FVLQ/Q/ TgFIX+ genotype was identified. When pregnancies were interrupted at embryonic age of E9.5 to E16.5, no deviation from the expected/observed embryo genotypes ratios was observed. However, the number of reabsorbed embryos increased significantly from 13% (E9.5) to 33% (E.16.5), p Disclosures: No relevant conflicts of interest to declare.