Francisco J. Sánchez Rivera1,2 and Lukas E. Dow3,4,5 1David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA 2Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA 3Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, New York 10065, USA 4Department of Biochemistry, Weill Cornell Medicine, New York, New York 10065, USA 5Department of Medicine, Weill Cornell Medicine, New York, New York 10065, USA Correspondence: fsrmit.edu; lud2005med.cornell.edu

Cancers arise through acquisition of mutations in genes that regulate core biological processes like cell proliferation and cell death. Decades of cancer research have led to the identification of genes and mutations causally involved in disease development and evolution, yet defining their precise function across different cancer types and how they influence therapy responses has been challenging. Mouse models have helped define the in vivo function of cancer-associated alterations, and genome-editing approaches using CRISPR have dramatically accelerated the pace at which these models are developed and studied. Here, we highlight how CRISPR technologies have impacted the development and use of mouse models for cancer research and discuss the many ways in which these rapidly evolving platforms will continue to transform our understanding of this disease.