For instance, it has been observed that the targeting of HIF-1α or HIF-2α by shRNA in CD133+ GSCs from a patient's glioblastoma specimen inhibited their neurosphere-forming ability and proliferation, induced the caspase-dependent apoptotic effect in vitro and attenuated their tumour-initiating potential in vivo [127, 148]. Here, EPAS1 is linked to neoplasm.