Over 80% of cancer fatalities are caused by aggressive and treatment-resistant forms of disease. While new targeted therapies and immunotherapies have significantly improved clinical outcomes in the last decade, but most patients ultimately succumb to their disease because of primary or acquired resistance. To develop more effective treatment strategies, it is critical to understand better the molecular drivers of cancer progression and therapeutic response. Cancer cells frequently exhibit high mutation rates due to extensive DNA damage from factors such as radiation, chemical exposure, or inherited genetic predispositions. These mutations typically impact two major classes of cancer-driving genes: oncogenes, which activate signal transduction pathways that promote cell proliferation or inhibit cell death, and tumour suppressor genes, which control pathways that induce cell cycle arrest, senescence, or apoptosis. Understanding how mutations in these key pathways contribute to cancer progression and resistance is essential for improving therapeutic interventions and patient outcomes. However, there is now strong evidence that the evolution, progression rates, and treatment responses of cancers are also associated with additional genetic events (eg. mutations, chromosomal loss/gains) impacting a class of genes termed disease modifiers, many of which function as epigenetic regulators of gene expression. One such modifier is kat5, which is lysine acetyltransferase, and Loss of kat5 is associated with growing number of cancer types. The inactivation of kat5 in mice was embryonically lethal. So basically limited in vivo model systems have limited information on the role of kat5 in development and disease. This lead to our hypothesis to find out if zebrafish offers an alternative model to investigate the impact of kat5 deficiency on zebrafish inflammatory responses. The association of kat5 with inflammation could be pivotal in understanding certain cancers such as liver cancer where tissue inflammation often predisposes individuals to early-stage cancer development. Thus, exploring the role of kat5 may offer valuable insights and potential targets for preventing cancer development and metastasis.