Our in vitro experimental data revealed that the activation of placental trophoblast PPARγ by RGZ was beneficial for exosome‐mediated preadipocyte differentiation, yet the clinical application of RGZ during pregnancy is contraindicated, not only because of associated cardiovascular events[29] but also because of the potential risk for major birth defects, stillbirth, and macrosomia‐related morbidity, as indicated by limited evidence from animal studies. This evidence concerns the gene PPARG and Stillbirth.