Fncd3b, or fibronectin type III domain-containing protein 3B, is an important regulator of metabolism. It has been associated with multiple biological pathways such as the AMP-activated protein kinase (AMPK) pathway, endoplasmic reticulum (ER) stress, the unfolded protein response (UPR), and the Wnt/β-catenin signaling pathway. Its dysregulation is linked to various diseases, highlighting its biological importance. Genetic models, especially knockout mouse models, are valuable for studying its functions [1,2,3].

In a study on alcoholic liver disease (ALD), hepatocyte-specific Fndc3b knockdown in C57BL/6 N mice showed that Fndc3b deletion aggravated alcohol-induced liver steatosis via AMPK inhibition and exacerbated ethanol-mediated lipid peroxidation. The study also revealed a connection between Fndc3b and ferroptosis, indicating that Fndc3b plays a critical role in preventing hepatic steatosis and ferroptosis in response to chronic alcohol consumption [1].

In conclusion, Fndc3b is involved in regulating metabolism-related biological processes. Its functions in preventing hepatic steatosis and ferroptosis in ALD, as revealed by gene-knockout mouse models, highlight its potential as a therapeutic target for this disease. Additionally, its association with multiple cancer-related processes in various cancers implies its significance in oncology research [1].