Factor VII (F7) is a serine protease that initiates the extrinsic pathway of blood coagulation. It circulates as an inactive zymogen that is activated to factor VIIa by factor Xa, XIIa, IXa, or thrombin [PMID:271951]. In the presence of tissue factor and calcium ions, factor VIIa converts factor X to factor Xa and factor IX to factor IXa, propagating the coagulation cascade [PMID:271951]. Plasma FVII concentrations are quantitative traits influenced by both genetic variants and epigenetic modifications at the F7 promoter 12. F7 promoter polymorphisms, including the A2 allele and -402G>A substitution, modulate FVII levels through alterations in transcriptional activity and DNA methylation patterns 1. Congenital F7 deficiency is an autosomal recessive bleeding disorder characterized by weak genotype-phenotype correlation and variable clinical manifestations ranging from asymptomatic to severe bleeding 3. F7 genetic variants influence circulating FVII levels and coagulation activation markers, with haplotype-dependent effects on coronary heart disease risk 4. F7 has minimal influence on coumarin anticoagulant dose requirements compared to CYP2C9 and VKORC1 5. F7 genetic polymorphisms may also influence COVID-19 disease severity 6.