Mice rarely develop melanoma spontaneously, but can be genetically manipulated (transgenic and/or knockout mice) to do so by activating oncogenes relevant to human melanoma, such as mutant BRAF or mutant NRAS, and/or via inactivation of key tumor suppressors, including CDKN2A or PTEN, i.e., they harbor defined genetic aberrations, which mimic the genetic lesions (or their consequences) that occur in human melanomas [45]. The gene discussed is CDKN2A; the disease is melanoma.