For example, the ability of TZD to inhibit cancer cell growth does not correlate with the levels of PPARγ expression, and there is a three orders of magnitude discrepancy between the concentration required to produce antitumor effects and that for PPARγ activation and also to modify insulin action [42], [43] Moreover it was possible to dissociate by structural modification the PPARγ activation and the antitumor effects in two prostate cancer cell lines [41]. This evidence concerns the gene PPARG and cancer.