Especially, in vivo, reduced tumor growth and microvessel numbers were observed in mice implanted with melanoma, Lewis lung carcinoma (LLC), fibrosarcoma, and glioblastoma due to a systemic treatment of PPAR alpha ligand, and the antiangiogenic state induced through activation of PPAR alpha with elevated thrombospondin-1 (TSP1) and endostatin expression [5]. The gene discussed is THBS1; the disease is Carcinoma, Lewis Lung.