Although IL - 1β represents a pivotal theoretical nexus linking depression and cancer, its clinical translation faces dual challenges: while mechanistic studies have confirmed that IL - 1β promotes lung cancer progression through activation of the NF-κB/AP-1 signaling pathways, induction of EMT, and metabolic reprogramming—such as inhibition of ferroptosis and enhancement of glycolysis—its elevation in depressive states exhibits pronounced heterogeneity. The gene discussed is NFKB1; the disease is depressive disorder.