Class II FINs target the t (4; 14) translocation–driven MMSET–ACSL4 axis to promote the synthesis of PUFA-PLs, thereby enhancing lipid peroxidation sensitivity. In combination with bortezomib, they further induce ferroptosis in t (4; 14)-positive MM cells by increasing Fe2+ release and suppressing GPX4-mediated antioxidant defense. Here, ACSL4 is linked to Miyoshi myopathy.