KLF11 is a zinc finger transcription factor that functions as a master regulator of cell proliferation, metabolic reprogramming, and ferroptosis 12. As a DNA-binding transcription factor, KLF11 activates epsilon- and gamma-globin gene promoters while repressing SP1-like binding sites and inhibiting cell growth 13. KLF11 regulates critical metabolic pathways by suppressing GPX4 to promote ferroptosis in lung adenocarcinoma 4 and by forming transcriptional complexes with PPARα to reprogram macrophage metabolism from glycolysis to fatty acid oxidation in atherosclerosis 5. In brown adipocytes, KLF11 cooperates with PPARγ to maintain brite-selective gene programs and mitochondrial oxidative capacity 6. KLF11 protects against diabetic atherosclerosis by inhibiting endothelial-to-mesenchymal transition and suppressing oxidative stress 7, and alleviates rheumatoid arthritis by downregulating YAP1 expression and M1 macrophage polarization 8. In sorafenib-induced cardiotoxicity, KLF11 promotes ferroptosis by suppressing FSP1 9. Disease-relevant mutations in KLF11 cause maturity-onset diabetes of the young 7 10. These findings establish KLF11 as a pleiotropic regulator with therapeutic potential across metabolic, cardiovascular, and oncologic diseases.