Facial infiltrating lipomatosis causes diffuse overgrowth of subcutaneous fat, muscle, and bone. Because adipose tissue mass is angiogenesis dependent, the purpose of this study was to determine whether neovascularization is upregulated in this disease.Infiltrating lipomatosis tissue was collected prospectively from the preauricular cheek of 5 patients; neovascularization was compared to normal postauricular adipose. Specimens were analyzed using immunofluorescence for CD31 (microvascular density), α-smooth muscle actin (pericyte marker), CD31/Ki67 (proliferating endothelial cells), and CD34/CD133 (endothelial progenitor cells). Quantitative reverse transcription-polymerase chain reaction was used to determine messenger RNA expression of progenitor cells (CD133) and factors that recruit them: vascular endothelial growth factor (VEGF-A), hypoxia-inducible factor 1α, matrix metalloproteinase 9 (MMP-9), and stromal cell-derived factor 1α. Angiopoietin 1 and 2, MMP-2, VEGF receptors, and neuropilin receptors were quantified using quantitative reverse transcription polymerase chain reaction. There was no difference in microvascular density, pericytic density, or endothelial proliferation between infiltrating lipomatosis and normal adipose tissue (P = 0.2). Expressions of VEGF-A, hypoxia-inducible factor 1α, stromal cell-derived factor 1α, angiopoietin 1 and 2, MMP-2 and -9, VEGF receptors 1 and 2, neuropilin receptors 1 and 2, and CD133 messenger RNA were not elevated compared to control fat (P = 0.1). Endothelial progenitor cells were not present in specimens of infiltrating lipomatosis. Infiltrating lipomatosis does not exhibit elevated angiogenic or vasculogenic factors compared to normal fat; the vasculature is stable. Neovascularization does not seem to play a role in the pathogenesis of this condition.