CDK4 and melanoma: Similarly, seeding human melanocytes transformed with mutated melanoma-associated genes, including N-RasG12V, CDK4R24C, and dominant-negative p53R248W, which are critical for p16INK4A-CDK4-Rb and ARF-HDM2-p53 tumor suppressor pathways, into autologous human skin grafts in immunodeficient mice results in the development of human melanocytic neoplasia in vivo, demonstrating the value of mouse models in the functional analysis and validation of mutations observed in human melanoma (53).