The liver is responsible for metabolism, digestion and nutrient storage, and unlike other human organs, it is able to remarkably regenerate following injury or partial removal. Healthy liver regeneration is driven by normally quiescent hepatocytes that rapidly proliferate following injury to restore tissue architecture and function. Impaired liver regeneration poses as significant clinical burden as treatment for patients with liver diseases such as hepatocellular carcinoma relies heavily on successful liver transplantation and regrowth. Liver regeneration is multifaceted, involving multiple cell types to sense injury and activate tissue regrowth responses. Consequently, understanding the cellular mechanisms and molecular underpinnings of liver regeneration is critical. Nrf2 is a transcription factor involved in sensing cellular stress and we have previously identified Nrf2 to be required for liver regeneration. We have preliminary data demonstrating that Nrf2 zebrafish mutants have impaired regeneration and wild-type larvae treated with the liver toxin acetaminophen (APAP) have increased expression of Nrf2 bona fide target genes compared to untreated larvae. Consequently, we aim to elucidate Nrf2’s role in remodelling the adaptive transcriptional landscape following liver injury and during regeneration. The development of a transgenic zebrafish whereby we can sort large numbers of hepatocytes from both larvae and adult zebrafish rapidly through magnetic activated cell sorting will uncover a temporal understanding of the transcriptional landscape and gain an insight into the chromatin interactions that are occurring in the context of Nrf2 following injury. Ultimately, we hope to identify new targets or pathways that Nrf2 may be co-opting with to driver liver regeneration.