The FGG gene encodes the fibrinogen gamma chain, a critical component of the fibrinogen complex that polymerizes with fibrinogen alpha and beta chains to form insoluble fibrin matrices essential for hemostasis and blood clot formation. FGG functions as a structural molecule in extracellular matrices and supports cell-matrix adhesion through integrin binding, facilitating cell migration during wound repair and re-epithelialization. Beyond hemostasis, FGG enhances platelet activation via ITGB3-dependent pathways and plays immunoprotective roles, including protection against infection-associated hemorrhage and facilitation of both innate and T-cell mediated antibacterial responses. Maternal fibrinogen is essential for successful pregnancy. Mutations in FGG cause congenital fibrinogen deficiency disorders, including afibrinogenemia and dysfibrinogenemia 1. These conditions present with variable bleeding severity; surprisingly, thrombotic events occur in approximately 10-11% of afibrinogenemic and hypofibrinogenemic patients 1. Pregnancy complications are particularly severe in dysfibrinogenemic women, with spontaneous abortion rates reaching 86% 1. Hotspot mutations at FGG p.Arg301Cys/His account for 51% of dysfibrinogenemia cases 1. Treatment relies primarily on fibrinogen concentrates administered on-demand or prophylactically, with efficacy correlating to factor activity levels in approximately 58% of cases 1.