Borobia et al. [100] developed an algorithm for a cohort of 147 patients with thromboembolic venous disease who were on stable doses including clinical variables (age, body mass index (BMI), amiodarone use, and enzyme-inducer use) and genetic variations of CYP2C9, VKORC1, CYP4F2, and APOE. The clinical factors explained 22% of the dose variability, which increased to 60.6% when pharmacogenetic information was included (p < 0.001) [100]. The gene discussed is CYP2C9; the disease is venous thromboembolism.