In CML, selinexor inhibits the nuclear export protein XPO1 to block the NF-κB signaling pathway, downregulate GPX4 expression, and activate NCOA4-mediated ferritinophagy. In combination with ferroptosis inducers, it enhances lipid peroxidation, thereby overcoming drug resistance and inducing ferroptosis. The gene discussed is NFKB1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.