MK2, a stress‐responsive kinase downstream of p38 MAP kinase, has been previously reported to promote the survival of cancer cells under various stimuli and chemotherapeutic resistance.[21, 22] Importantly, its major substrate, HSPB1 (also called HSP27), negatively regulates ferroptosis by reducing intracellular iron accumulation and uptake.[23, 24, 25] Therefore, we aimed to confirm whether MK2 was an essential downstream mediator of COPS5 function in ferroptosis resistance. The gene discussed is HSPB1; the disease is cancer.