F5 and Thromboembolism: FV mutation involves a G-A substitution at nucleotide 1691, resulting in a pro-coagulant state by inducing FV resistance to inactivation by protein C, and FV G1691A mutation was one of the most common genetic risk factors for thromboembolism in Western countries.[16] Moreover, the relationship between risk for VTE and FV gene polymorphisms may differ depending on different genotypes.[11]