Taken together, the available data appear to be consistent with a model in which Myc proteins function downstream of D-type cyclins and synergize with E2F proteins in the activation of the cyclin E/cdk2 kinase. This view of Myc proteins appears strikingly similar to established models for the E2F/DP family of proteins. However, it should be noted that there are clear differences and several predictions of such a model that have been critically tested for E2F proteins are still untested for Myc in this model. First, it appears that at least some target genes of Myc implicated in this process are still unknown; second, clear data from knockout cells that link p107 to Myc function are missing; and third, we are not aware of studies of tumour samples that clarify whether mutations in myc genes relieve the requirement for mutations in the cyclin D/p16 pathway.