These findings lend support to the mounting evidence that Arf can, in part, function as a tumor suppressor independently of its role in modulating p53 activity, and support the growing paradigm that oncogenes/tumor suppressors regulate tumor progression not only via disrupting the balance between homeostatic proliferation/apoptosis but also via eliciting adaptation of the tumor microenvironment to support neoplastic growth. This evidence concerns the gene CDKN2A and neoplasm.