FOXC2 is a member of forkhead/winged helix transcription factor family, whose members serve as key regulators in embryogenesis and cell differentiation (3). FOXC2 functions as a key regulator of adipocyte metabolism by increasing the sensitivity of the beta-adrenergic-cAMP-protein kinase A (PKA) signaling pathway through alteration of adipocyte PKA holoenzyme composition (4). Increased FOXC2 levels, induced by high fat diet, seem to counteract most of the symptoms associated with obesity (4). FOXC2 expression is also associated with the early stage of chondrogenic differentiation both in vivo and in vitro (3). FOXC2 haploinsufficiency results in Lymphedema-distichiasis (LD), an autosomal dominant disorder that classically presents as lymphedema of the limbs, and double rows of eyelashes (distichiasis) (5). Mutant mice null for FOXC2 show defects in axial and cranial skeletogenesis, suggesting a requirement of FOXC2 for skeletal tissue development (3). FOXC2 interacts with FOXC1 in the Notch signaling pathway (1) and in kidney and heart development (2).