Anyway, some colorectal cancer cell lines are resistant to PPARγ agonists, because elevated PPARδ expression and/or activation of PPARδ antagonize the ability of PPARγ to induce colorectal carcinoma cell death, as a result of opposing effects of PPARδ and PPARγ in regulating programmed cell death mediated by survivin and caspase-3: activation of PPARγ results in decreased survivin expression and increased caspase-3 activity, whereas activation of PPARδ counteracts these effects [36]. This evidence concerns the gene CASP3 and colorectal cancer.