Activated FVII binds to endothelial protein C receptor (EPCR), which enhances hemostasis.14 One study showed that eptacog beta binds to EPCR with 25% to 30% more affinity than eptacog alfa, displacing protein C from EPCR binding sites and downregulating activated protein C generation, contributing to its hemostatic effect. Physiology
The main role of factor VII (FVII) is to initiate the process of coagulation in conjunction with tissue factor (TF/factor III). Tissue factor is found on the outside of blood vessels - normally not exposed to the bloodstream. Upon vessel injury, tissue factor is exposed to the blood and circulating factor VII. Once bound to TF, FVII is activated to FVIIa by different proteases, among which are thrombin (factor IIa), factor Xa, IXa, XIIa, and the FVIIa-TF complex itself. The complex of factor VIIa with TF catalyzes the conversion of factor IX and factor X into the active proteases, factor IXa and factor Xa, respectively.The action of the factor is impeded by tissue factor pathway inhibitor (TFPI), which is released almost immediately after initiation of coagulation. Factor VII, which was discovered around 1950, is vitamin K-dependent and produced in the liver. Use of warfarin or similar anticoagulants decreases hepatic synthesis of FVII. Structure
Factor VII shares a common domain architecture with factors IX and X.

Genetics
The gene for factor VII is located on chromosome 13 (13q34). Role in disease
Factor VII deficiency (congenital proconvertin deficiency) is rare and inherited recessively. It presents as a hemophilia-like bleeding disorder. It is treated with recombinant factor VIIa (NovoSeven or AryoSeven).
Symptoms affecting quality of voice tend to worsen after speaking for long periods of time, or when speaking with increased volume. Many individuals who use their voice professionally find even a slight presence of symptoms to be problematic. However, some voice professionals are not impacted by the presence of vocal cysts. Vocal Dynamics
Vocal fold cysts cause the properties of the vocal folds to change. When a cyst is present on a vocal fold, the cover of the vocal fold becomes more stiff and increases in mass. The increased mass and stiffness tends to result in hyperkinetic muscular movement during phonation. Hyperkinetic movement is characterized by increased rigidity in the affected vocal fold(s). This hyperkinetic movement results in the voice being perceived as hoarse. (see Signs and Symptoms) Specifically, the presence of a vocal fold cyst leads to an asynchronous mucosal wave of the vocal folds during phonation. Causes
There are several possible causes of vocal fold cysts: 

They can be congenital. They can result from the blockage of a mucous glands excretory duct. In this case, they are sometimes referred to as retention cysts. They can be the result of phonotrauma. Phonotrauma refers to behaviours that can lead to vocal fold injuries, such as vocal overuse (i.e. too much speaking), vocal misuse (i.e. speaking in an unnaturally high or low pitch), or vocal abuse (i.e. yelling or whispering for prolonged periods). Vocal folds vibrate during phonation resulting in repeated collisions of the right and left vocal folds.