Cancer is a multifaceted disease involving changes at the genomic, cellular, and eventually at the organismic level. Fundamentally, cancer originates in the genome, by mutations that either activate oncogenes or inactivate tumor suppressors. Dysregulation of the epigenome is another feasible way by which cells can become cancerous due to altered expression of certain genes involved in DNA damage pathway or cell cycle pathway. At cellular level, cancer results in altered metabolism, altered cell structure and migration which enables growth of cancer cells in unfavorable environments. Eventually, in the affected organism, cancer cells circumvent the immune defense mechanism of the host and co-exist with normal cells. Understanding of all these complex genomic, cellular, and tissue level changes is crucial for the development of more effective treatment options and improving outcomes in cancer patients. CRISPR/Cas technology has had a significant impact on our understanding of cancer biology and is continuously driving new discoveries in the field. Supplementary Figure shows the publication trend of CRISPR-related publicationsjournals and patents for different cancers subtypes (both solid cancer and hematological malignancies). Increase in journal publications was most prevalent/evident for breast cancer, acute myeloid leukemia (AML), liver, lung and rectal cancer. In line with the journal publications, patent publication trends show breast cancer, AML, lung and liver cancer related patents to be growing rapidly indicating potentially more commercialization efforts for these cancer types. Other cancer types with rapid increase in CRISPR patents include melanoma. Multiple gene candidates are being studied in cancers in context of CRISPR. Figure below shows co-occurrences between cancer types and genes found in the CRISPR dataset retrieved from CAS Content Collection. A few key observations from this co-occurrence analysis are as follows: