Ketohexokinase (Khk), also known as fructokinase is the first enzyme in a specialized catabolic pathway metabolizing dietary fructose to the glycolytic intermediate glyceraldehyde-3-phosphate. While the metabolic mechanism of glucose is tightly regulated by feedback mechanism, the metabolic mechanism of fructose bypasses feedback inhibition. Studies on metabolism of fructose have recently garnered attention due to the association of high fructose diets with an increased risk of diabetes and other diseases. These adverse effects in both human and animal models were exhibited during adult stage. However, the impact of fructose diet and Khk on fetal development has been overlooked. We utilized zebrafish as an animal model to study Khk function during early embryonic development. We utilized zebrafish as an animal model to study Khk function during embryonic development. mRNA of Khk is detected as early as 1-cell stage and an alternative transcript is detected from 10 to 48 hours post fertilization (hpf). We designed two morpholinos to block either translation or splicing of khk and injected into newly fertilized embryo. Knockdown (KD) of khk results in fused somites and defective intersomatic vessel (ISV). Utilizing CRISPR/Cas9 system we edit khk genomic DNA and observe similar phenotype to morpholino-based KD of khk. Taken together, these data suggest a role for khk in early embryonic development, especially in somatogenesis and angiogenesis. .