HIF1A and neoplasm: Therefore, we propose a context‐dependent model: in acute hypoxia (short‐term oxygen fluctuations) or in vitro nutrient sufficiency, HIF‐1α supports NK cell survival and activation, whereas in chronic hypoxia (prolonged oxygen deprivation), combined with resource exhaustion and activation of tumor‐promoting signaling pathways, HIF‐1α drives NK cell metabolic dysfunction.