KLF10 is a zinc finger transcription factor that functions primarily as a TGF-β-inducible transcriptional regulator with context-dependent roles in metabolism, fibrosis, and muscle homeostasis 1. As a downstream mediator of TGF-β/SMAD signaling 2, KLF10 binds GC-box sequences to regulate gene expression across multiple tissues. In hepatic metabolism, KLF10 protects against metabolic dysfunction-associated steatohepatitis by inducing HNF4α expression, promoting fatty acid oxidation, and inhibiting lipogenesis 3. Conversely, KLF10 mediates cancer cachexia through a TGF-β/KLF10 axis that upregulates atrophy-associated ubiquitin ligases Trim63 and Fbxo32, with KLF10 knockout mice showing preserved lean mass in pancreatic cancer models 4. KLF10 demonstrates tissue-specific and context-dependent fibrotic effects 5. In CD4+ T cells, KLF10 suppresses IL-9 transcription through HDAC1 interaction; KLF10 deficiency increases IL-9-mediated fibroblast activation, exacerbating perivascular fibrosis and organ dysfunction 6. In kidney proximal tubule cells, KLF10 functions within a transcription factor network (ELF3/KLF6/KLF10) regulating health-to-injury transitions 7. These findings suggest KLF10 as a pleiotropic regulator with therapeutic potential in metabolic, fibrotic, and cachectic diseases.