Phenotyping of both cell types in primary BC has demonstrated a discordant estrogen receptor (ER), progesterone receptor (PR), and/or HER2 receptor status between the primary tumor and these cells and that a proportion of DTCs and CTCs are nonproliferative and stem cell–like as well as being in epithelial–mesenchymal transition (EMT), which may explain resistance to antihormonal and conventional chemotherapeutic drugs [31–40]. The gene discussed is PGR; the disease is breast cancer.