Despite a vaccine being available, human papillomavirus virus (HPV)-driven cancers remains the ninth most prevalent cancer globally. Current therapies have significant drawbacks and has, generally still leading to poor prognosis and underwhelming survival rates. With gene therapy becoming more available in the clinic, it poses a new front for therapeutic potential. A characteristic of HPV driven cancers is its ability to encode oncoproteins that aberrate normal p53 function without mutating this tumour suppressor gene. The HPV E6 oncoprotein degrades p53 to allow HPV-driven carcinogenic process to proceed. Following the advent of clustered regularly interspaced short palindromic repeats (CRISPR), such gene editing technology may be adopted to overcome HPV-mediated silencing of p53 by hyper expressing the p53 promoter. Increasing p53 bioavailability remains a promising potential therapy and has been a goal in the context of HPV driven cancers. Clinical trials and proof-of-concept pre-clinical work has shown positive outcomes and tumour death when p53 are levels are increased. Despite previous successes of RNA-based medicines, including the knockout of HPV’s crucial oncogenes, the use of CRISPR activation (CRISPRa) is yet to be investigated as a potential promising therapy. This project aims to explore the use of CRISPR activation to hyperactivate p53 to overcome HPV E6s mediated silencing and investigate the effects of increased p53 levels in cervical cancer.