We hypothesize that the net effect of thiazolidinedione in cancer cells depends on the balance of PPARγ-mediated (prooncogenic) and PPARγ-independent (antioncogenic) mechanisms, by means of regulation different factors including receptor expression levels, phosphorylation status, expression of the heterodimeric partners, and the presence of endogenous ligands. The gene discussed is PPARG; the disease is cancer.