“…The pharmacokinetics and pharmacodynamics of this drug are affected by functional polymorphisms in both CYP2C9 and VKORC1 genes [10,11]. The polymorphic variants in both genes independently correlate with the clinical dose of acenocoumarol [12] and the time required to achieve an effective dose for stable anticoagulation [12][13][14].The combination of two polymorphisms in CYP2C9 and VKORC1 could explain between 25 and 40% (20-25% for VKORC1 and 5-15% for CYP2C9) of the variability in therapeutic doses of coumarins as acenocoumarol [15,16], whereas the combination of demographic, clinical and genetic factors explains 45-55% of the total variation in the optimal therapeutic dose [1,8,[17][18][19][20][21][22].There are several pharmacogenetic models found in the literature for predicting the optimal warfarin dose for various population groups. However, there are limited papers on optimal acenocoumarol dose.…”