Since HIF-1β is an indispensable dimer partner for both HIF-1α and HIF-2α, no functioning HIF-1 or HIF-2 complexes are formed in Hepa-c4 cells [14,15], making them a good model for a tumour that has become resistant to either anti-HIF-1 or anti-HIF-2 agents, or to agents that simultaneously inhibit HIF-1 and HIF-2. The gene discussed is HIF1A; the disease is neoplasm.