Based on our results we propose the following hypothesis (Figure 7): In U2OS cells, and perhaps in other cancer cells with dysregulated proliferation, we envision that under normoxia, a transactivating complex consisting of Miz-1/Arnt and perhaps Hif1α or Hif2α is anchored on the CDKN2B proximal promoter via the DNA binding domain of Miz-1, stimulating expression of CDKN2B. The gene discussed is EPAS1; the disease is cancer.