KLF11 is a zinc-finger transcription factor that regulates diverse cellular processes including cell growth, apoptosis, and metabolic programming. As a sequence-specific DNA-binding protein, KLF11 activates epsilon- and gamma-globin gene promoters while repressing SP1-like binding sites and inhibiting cell proliferation. In pancreatic beta cells, KLF11 acts as a glucose-inducible regulator of the insulin gene promoter 1, and rare missense variants (Ala347Ser, Thr220Met) segregating with early-onset type 2 diabetes significantly impair its transcriptional activity; a common Gln62Arg polymorphism associates with type 2 diabetes in North European populations and reduces insulin expression 1. Beyond glucose homeostasis, KLF11 coordinates metabolic and inflammatory processes. In adipocytes, it functions as a browning factor required for PPARγ agonist-induced activation of mitochondrial oxidative capacity 2. In macrophages, KLF11 suppresses M1 polarization by downregulating YAP1 and reducing atherosclerotic lesion formation 34. In cancer contexts, KLF11 promotes ferroptosis—an iron-dependent cell death pathway—by suppressing the ferroptosis regulators GPX4 and FSP1, thereby inhibiting lung adenocarcinoma proliferation and enhancing chemotherapy sensitivity 56. Clinically, low KLF11 expression in lung adenocarcinoma correlates with reduced patient survival 5. In diabetic atherosclerosis, endothelial KLF11 protects against endothelial-to-mesenchymal transition and oxidative stress under hyperglycemic conditions 7. These findings identify KLF11 as a pleiotropic regulator with therapeutic potential in metabolic and cardiovascular diseases.