Hemostasis is a crucial function that prevents blood loss after vascular injury by forming platelet-fibrin clots. Disruptions in this process can cause bleeding or thrombotic disorders like hemophilia, von Willebrand disease, or acquired coagulopathies. Zebrafish (Danio rerio) have become an alternative animal model to study mammalian hemostasis disorders. This study focuses on four bleeding disorders, namely Bernard-Soulier syndrome, hemophilia A, hemophilia B, and parahemophilia. To this end, we utilized gp1ba, fv, and fviii mutants with premature stop codons from the Zebrafish International Resource Center (ZIRC), initially obtained as heterozygote and wild-type embryos. After three months of growth, the adults were genotyped and subsequently bred to homozygosity. Through a series of functional assays, we systematically characterized these mutants, identifying phenotypic parallels to the human conditions, Bernard-Soulier syndrome, parahemophilia, and hemophilia A. Previous research in our laboratory identified hemostatic functions for three f9 genes in zebrafish: f9a, f9b, and f9l. Given the absence of knockout models to support these findings, I developed a zebrafish model for hemophilia B by targeting the f9a gene, which is analogous to the human FIX gene. We disrupted the catalytic domain using CRISPR/Cas9 technology at two sites within exon 8, mirroring a common mutation site found in hemophilia B patients. This 72 bp deletion caused prolonged bleeding times and disrupted intrinsic pathways, as verified by the kPTT (kinetic partial thromboplastin time) assay. Western blot and quantitative RT-PCR analyses also confirmed reduced F9a protein and f9a RNA levels. Also at the larval stage, mutants exhibited an extended time to occlusion following venous caudal laser injuries. We also generated an f9l knockout model (functionally linked to the human FX gene), using CRISPR/Cas9 technology to target exon 8. The resulting knockout model had a complex mutation that showed impaired coagulation, confirmed by the kRVVT (kinetic Russell’s viper venom time) assay. Larval studies revealed incomplete penetrance of prolonged bleeding, suggesting intervention by compensatory mechanisms. Unlike f10 zebrafish, f9l mutants exhibited partial lethality, with some mutants surviving beyond nine months. Downregulating f10 in f9l homozygous embryos using morpholinos resulted in 50% mortality within 24 hours, highlighting a functional relationship between f9l and f10. In summary, this comprehensive study advances our understanding of hemostasis in zebrafish, by contributing significantly to the field by establishing models for Bernard-Soulier syndrome, hemophilia A, parahemophilia, and hemophilia B, and by elucidating the role of f9l. These findings provide a solid foundation for future generations of suppressor mutations and gene therapy, offering a robust platform for exploring gene regulation in coagulation and hemostasis.