In addition to genetic mechanisms that can irreversibly affect the balance of HIF-1α and HIF-2α activities, such as loss of one copy of chromosome 14q, encoding HIF1A, or intragenic deletions of HIF1A22, several mechanisms exist that potentially provide tumour cells with a more dynamic mode of fine-tuning the relative strengths of HIF-1α and HIF-2α expression and activities. Here, EPAS1 is linked to neoplasm.