Factor XI (F11) is a serine-type endopeptidase that functions as a key activator in the intrinsic pathway of blood coagulation. It triggers the middle phase of coagulation by activating factor IX, a critical step in the coagulation cascade. F11 also participates in fibrinolysis regulation and is present in plasma and extracellular compartments 1. F11 deficiency is a recognized bleeding disorder with variable clinical manifestations depending on factor levels. Notably, the correlation between F11 levels and bleeding phenotype is less predictable than in other coagulation deficiencies, making bleeding risk assessment challenging 1. The condition has particularly high prevalence in Ashkenazi Jewish populations, though it is increasingly diagnosed across other ethnic groups. Beyond its classical coagulation role, F11 has emerged as a therapeutic target in thromboembolic disease. Proteome-wide Mendelian randomization studies identified F11 as a causal protein associated with venous thromboembolism (VTE) development, with strong genetic support for this association 2. Additionally, F11 was identified as a potential drug target specifically for cardioembolic stroke, with multiple drug candidates currently in development 3. Recent evidence also suggests F11's involvement in hepatocellular carcinoma pathogenesis through fatty acid metabolism-related pathways 4, though its precise mechanistic role in malignancy requires further investigation.