HIF2α promotes RCC tumor growth by increasing c-Myc transcription activity that promotes cell cycle progression and cellular proliferation, whereas HIF1α antagonizes c-Myc function by displacing c-Myc from p21cip1 promotor, leading to the activation of the cyclin-dependent kinase (CDK) inhibitor p21cip1 that causes cell cycle arrest in G1 phase or in the G2/M transition after DNA damage [51,52]. The gene discussed is EPAS1; the disease is neoplasm.