Abstract: fbxo32, a muscle-specific E3 ubiquitin ligase, can enhance protein degradation to associate with atrophy. Here, we found that traf6 mutant zebrafish liver fbxo32 mRNA level increased dramatically. To find out the role of fbxo32 in liver disease, we performed histological analysis of mutant and wildtype zebrafish liver. The result showed that the mutant liver exhibited apparent characteristics of liver atrophy, such as loose liver tissue structure, irregular arrangement and rare lipid droplets of the hepatocytes. The qRT-PCR result showed that fbxo32 mRNA was widely expressed in most tested tissues with the highest level in ovary and low level in liver of wildtype zebrafish. Especially, compared with the wildtype, the liver fbxo32 mRNA was elevated about 100 folds in the traf6 mutant. Additionally, fbxo32 mRNA was mainly distributed in hepatocytes based on in situ hybridization, but cannot be detected in blood cells. The signal of fbxo32 mRNA was much stronger in traf6 mutant liver. These findings indicate that the knockout of traf6 might induce the expression of fbxo32 mRNA in liver and result in liver developmental abnormality and atrophy.