Traditionally, cancer has been understood as a genetic disease, driven by mutations that accumulate over time. However, recent discoveries challenge the exclusive role of genetics in driving tumourigenesis. For example, studies have identified ostensibly healthy human tissue harbouring multiple tumour-initiating mutations, whilst genetically engineered mouse models have revealed that oncogenic mutations are necessary but not sufficient to drive tumour initiation. These studies highlight the crucial role of non-genetic factors in enabling cells to become competent for tumour formation. This has led to the concept of ‘oncogenic competence’, which describes the phenomenon where the tumorigenic potential of an oncogene depends on specific cellular context and environmental factors. Liver cancer represents a compelling model to study oncogenic competence, as genomic sequencing of histologically normal liver biopsies have revealed a high mutational burden that includes oncogenic mutations. In our studies, we have employed a novel zebrafish model of liver cancer (p53KO; TO:YAP) that recapitulates features typically observed in the clinical setting. This model combines a loss-of-function mutation in p53 with a hepatocyte-specific doxycycline-inducible expression of the oncogene YAP. Using this conditional model of liver cancer we have defined that developmental age determines oncogenic competence. Specifically, induction of YAP during the early stages of embryogenesis leads to profound tumour formation, whereas induction of YAP at later stages of development has no tumorigenic effect. We have deployed a combination of unbiased transcriptomic approaches (SLAM-IT Seq) to investigate the molecular underpinnings of age-dependent oncogenic competence. Our preliminary studies suggest that the metabolic poise of the liver regulates the ability of oncogenes to initiate liver tumours.