Congenital fibrinogen disorders are traditionally described as rare monogenic conditions caused by pathogenic variants in FGA, FGB, and FGG. However, increasing availability of large-scale genomic sequencing data and detailed molecular investigation has challenged this view. This thesis re-evaluates the prevalence and genetic complexity of congenital fibrinogen disorders by integrating population-scale analyses, detailed case-based studies, and functional investigation, suggesting that these disorders may be less rare and less strictly monogenic than previously assumed.