FOXC1 is a forkhead box transcription factor that functions as a DNA-binding regulator acting either as a transcriptional activator or repressor 1. It binds consensus sequences in target gene promoters and promotes DNA bending upon binding 1. FOXC1 plays essential roles in multiple developmental processes including eye, bone, cardiovascular, kidney, and skin development 1. Mechanistically, FOXC1 regulates endochondral ossification through cooperation with GLI2 in hedgehog signaling and maintains cell viability through FOXO1 regulation 1. It also promotes epithelial-mesenchymal transition and induces cell cycle arrest in the G1 phase via TGFB1-mediated signals, suggesting tumor suppressor potential 1. In disease contexts, FOXC1 mutations cause anterior segment dysgenesis and Axenfeld-Rieger syndrome 1. FOXC1 is significantly overexpressed in triple-negative breast cancer (TNBC) and serves as a highly specific diagnostic marker for the triple-negative phenotype 2. In TNBC, FOXC1 expression associates with aggressive tumor phenotypes and is regulated by TNBC-specific super-enhancers 3. Additionally, FOXC1 loss in valvular endothelial cells causes myxomatous mitral valve degeneration through disrupted junctions and lymphatic vessel dysfunction 4. Recent evidence demonstrates FOXC1 regulates insulin signaling genes (Insr, Irs1) in skeletal muscle, contributing to metabolic health 5. FOXC1 functions as a conserved oncogenic driver in TNBC parallel to FOXA1 in estrogen receptor-positive breast cancer, cooperating with nuclear receptor NR2F2 6.