Mechanistically, FSP1+ cells in B16F10 tumor sections showed strong TGF-β1 immunoreactivity, and treatment of primary mouse lung endothelial cells (MLECs) with TGF-β1-induced spindle-like morphological changes, decreased CD31, and increased FSP1, consistent with TGF-β-driven EndMT. The gene discussed is S100A4; the disease is neoplasm.