The F7 antibody, primarily associated with acquired Factor VII (FVII) deficiency, is an autoantibody targeting coagulation Factor VII, a critical serine protease in the extrinsic blood clotting pathway. This rare condition often arises in autoimmune disorders, malignancies, or idiopathic cases, though drug-induced antibodies (e.g., from bovine thrombin exposure) have also been reported. FVII autoantibodies, typically IgG-type, neutralize FVII activity by blocking its interaction with tissue factor (TF) or accelerating its clearance, leading to impaired thrombin generation and bleeding manifestations ranging from mild mucosal bleeding to life-threatening hemorrhage. Diagnosis involves prolonged prothrombin time (PT) with normal activated partial thromboplastin time (APTT), confirmed by FVII activity assays and Bethesda-style inhibitor titration. Management includes immunosuppression (corticosteroids, rituximab), bypassing agents (activated prothrombin complex concentrates, recombinant FVIIa), and plasma exchange in acute settings. Research into F7 antibodies has advanced understanding of autoimmune coagulopathies, highlighting molecular epitope diversity and mechanisms of immune-mediated clotting dysfunction. Their study also contributes to therapeutic innovations, such as engineered FVII variants resistant to antibody inactivation, bridging hematology and immunology in translational medicine.