Oncogenes and tumor suppressor genes play a critical role in the process of tumorigenesis. There are known driver mutations which either activate the oncogenes or suppress the tumor suppressor genes, and both these phenomena disrupt the normal growth signaling pathways in cells, making them grow uncontrollably. Several studies have shown that by using CRISPR, it is possible to edit these mutations and revert the cancerous phenotype in vitro as well as in vivo. used CRISPR/Cas9 mediated gene editing to target mutations in c-Ki-Ras (KRAS) oncogene (KRAS G12C, G12D and G12V) in pancreatic cancer cells in mice and found that it inhibited cancer cell proliferation without affecting wild type cells. In other studies, CRISPR/Cas9 was used to knock out another mutant oncogene, epidermal growth factor receptor (EGFR), resulting in the inhibition of proliferation of lung adenocarcinoma cell lines and considerable decline in tumor size and weight in xenograft mouse models. TP53 gene codes for a transcription factor and a well-known tumor suppressor that regulates multitude intracellular pathways involved in DNA damage repair, cell cycle arrest, apoptosis, and senescence. Mutations in TP53 leading to its inactivation are involved in tumorigenesis and are found to be prevalent in more than 50% of human primary tumors. Majority of TP53 mutations are missense mutations (around 80%) occurring due to G to A transitions, followed by C to T transitions. These are clustered in the central DNA-binding region consisting of exons 3-5. Other known TP53 mutations are truncating mutations, in-frame mutations, and slice site alterations. Since majority of mutations are missense, it opens great opportunities for the CRISPR/Cas9 system to correct single nucleotides. In prostate cancer cell lines, the TP53 414delC mutation was corrected to the wildtype TP53 genotype by using the CRISPR/Cas9 system, thereby promoting apoptosis and preventing tumor proliferation. Zhan et al. have designed and constructed a genetic sensor that specifically detects wt-p53 expression in cells. Furthermore, by combining the p53 sensor with diphtheria toxin using the CRISPR/Cas9 system they were able to specifically kill p53-deficient tumor cells. proposed a novel and highly tumor specific TP53 delivery system based on CRISPR/Cas9 genome editing technology which can be used to replace the mutant TP53 in the tumor genome with a functional copy by homologous recombination, leading to sustained expression of p53 protein and tumor regression.