Abstract: Liver fibrosis is a progressive chronic liver disease that transitions from chronic inflammation to cirrhosis. In the absence of timely and accurate diagnosis and intervention, advanced liver fibrosis can lead to cirrhosis, liver failure, portal hypertension, often necessitating liver transplantation. Although liver tissue biopsy serves as the current gold standard for diagnosing liver fibrosis, its limitation in comprehensively examining all lesions poses a challenge to non-invasive assessments. Fibroblast activation protein (FAP) plays a pivotal role in liver fibrosis promotion and is closely associated with disease progression. Therefore, the potential of non-invasive FAP-targeted diagnostic nuclear medicine presents a promising avenue for precise diagnosis and staging of liver fibrosis. In this study, varying severity levels of liver fibrosis models were successfully induced in mice through intraperitoneal injection of carbon tetrachloride. The TEFAPI-12, derived from FAPI-46, exhibited specific uptake at fibrotic liver sites when used for PET imaging with a ⁶⁸Ga-labeled FAPI probe. The uptake intensity increased proportionally with the severity of fibrosis. The process of liver fibrosis involves intricate molecular changes correlated with disease progression. The correlation observed between liver ⁶⁸Ga-TEFAPI-12 uptake and the severity of liver fibrosis underscores the crucial role of ⁶⁸Ga-FAPI PET in diagnosing and staging liver fibrosis. This non-invasive approach holds great promise for improving the accuracy of liver fibrosis assessments and enhancing our understanding of the disease at a molecular level.