Although breast cancer has conventionally been classified based on the presence or absence of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), recent studies have indicated that the genomic landscape of breast cancer extends far beyond these 3 receptors.1 Genomic profiling of tumor specimens has helped identify other targets that may serve as driver mutations for the development of breast cancer, contributing to the heterogeneity of this disease.1–4. This evidence concerns the gene PGR and breast cancer.