OTUD5, a member of the ovarian tumor family, has recently emerged as a critical regulator in various diseases and pathological processes, including Primary Biliary Cholangitis,[45] embryogenesis,[46] inflammatory bowel disease,[47] DNA repair,[22] and immune response.[24] Interestingly, our RNA‐seq data indicated that the deubiquitinase enzyme OTUD5 depletion resulted in increased ferroptosis, and SLC7A11/SLC3A2 complex was significantly decreased in siOTUD5 cardiomyocytes. The gene discussed is SLC3A2; the disease is ovarian neoplasm.