In NSCLC and other malignancies, persistent STAT3 activation upregulates its downstream effector MCL1 (a member of the BCL-2 family), which sequesters BECN1 away from SLC7A11 and thereby preserves system Xc− function and ferroptosis resistance [14,15]. The gene discussed is SLC7A11; the disease is non-small cell lung carcinoma.