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Knockout of many of the remaining coagulation factors in the blood results in a bleeding phenotype that can be observed immediately.[12] This bleeding is called hemophilia A. In Africa and India, hemophilia A is more common, especially in isolated rural populations. In many cases, this is due to an inactive coagulation factor VIII gene [3]. Primary microcephaly type 2 (MCPH2) is a condition that affects the brain of the growing child. Instead of forming a full brain, the head of the infant, while growing, is underdeveloped.[10] MCPH2 is caused by mutations in the coagulation factor 8 gene (F8) [9] and occurs in many different populations, including in India in Pathakalipura, a small village in South India. F8 hydrocephalus, very rare and autosomal recessive, results from a mutation in the F8 gene, which codes for the protein coagulation factor VIII. The severity of the head defect is determined by the mutation (Ala119Glu, Thr600Met, Arg1701His, and Ala631Arg).[11]

The plasma protein factor VIII serves as a cofactor for plasma activated factor IX, it forms a complex with factor IXa that cleaves factor X (FX) into FXa to stimulate the production of thrombin. Thrombin activates FXII to FXIIa. In addition to its activity in the formation of hemostasis, FXII can activate C4 and FI, both involved in the complement system, which can activate thrombin generation and cleave fibrinogen to form fibrin.[8][9]

Fibrinogen is a 340 kDa protein for which there are three genes for clones [13,14]. The gene that codes for fibrinogen contains 11 exons, with regions that can be alternatively spliced at two sites and it codes for a single chain of polypeptide composed of three Aalpha/Bbeta/gamma dimers. Mutations in fibrinogen form cause fibrinogen disorders, most of which are autosomal recessive.

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