The activation of PPAR-γ by PGZ can halt the progress of breast cancer via multiple mechanisms, targeting estrogen receptor (ER) and aromatase, either by inhibiting ER expression through the PTEN pathway or inducing proteasome-dependent degradation of ER, or inhibiting aromatase via the PGE2 and BRCA1 pathways (139). This evidence concerns the gene ESR1 and breast carcinoma.