A recent study has shown that in two hormone-dependent breast cancer cell lines (MCF-7 and ZR-75-1), PPARγ activation could lead to ERα downregulation through the proteasome-dependent degradation pathway [65]; yet different PPARγ agonists exerted differential effects on ERα stability: troglitazone, ciglitazone, and natural PPARγ ligand 15d-PGJ(2) induced ERα degradation efficiently while rosiglitazone did not alter ERα protein levels [65]. The gene discussed is PPARG; the disease is breast cancer.