HMA reduces the viability of breast cancer cells of differing molecular profiles with equal efficiency [17], which is significant as breast cancer subtypes (luminal or basal, estrogen/progesterone receptor-positive (ER/PR+), HER2−amplified (HER2+), or receptor-negative (ER/PR/HER2−)) are variably resistant to chemotherapeutics and targeted drugs [18]. This evidence concerns the gene PGR and breast cancer.