Strikingly, TZD treatment resulted more effective in PPARγhep−/− mice than in WT mice [142], highlighting that (i) TZD antitumor activity is independent of PPARγ; (ii) PPARγ expression reduced TZD activity; therefore in this model PPARγ may support, rather than inhibiting, tumor growth. The gene discussed is PPARG; the disease is neoplasm.