When hypoxic breast tumor cells are exposed to pioglitazone (PPARγ agonist) and/or 6-OH-11-O-hydrophenanthrene (RXR agonist), the resultant exosomes are unable to trigger CAF activation compared with exosomes from tumor cells subjected to the control treatment, suggesting that these NR agonists can disrupt the tumor-stroma crosstalk [70]. The gene discussed is PPARG; the disease is neoplasm.