PPARγ activation with n-3 fatty acid docosahexaenoic acid (DHA) in vivo inhibited tumor vascularization and progression in a IL-17 dependent manner, but failed to reduce tumor vessel formation and growth in immunodeficient or IL-17 knockout animals, suggesting that the tumor angiogenesis inhibiting effects of PPARγ activation depend on T cells and the secretion of the pro-inflammatory cytokine IL-17 [66]. The gene discussed is IL17A; the disease is neoplasm.