Recent studies that have included more detailed characterization of tumor markers suggest that differences in risk factor associations between luminal A cancers (ER and/or progesterone receptor (PR) positive and human epidermal growth factor receptor 2 (HER2) negative) and core basal phenotype (CBP) cancers ("triple negative" for ER, PR and HER2 with expression of basal cytokeratins or epidermal growth factor receptor (EGFR)) account for much of this etiological heterogeneity. This evidence concerns the gene ESR1 and cancer.