Both interventions are based on the actions of estrogens, particularly on ERα, which is known to promote proliferation of breast cancer cells, and/or progestins, which activate not only the nuclear PR isoforms A and B, known to exert distinct effects on breast cancer growth, but also more recently identified membrane progesterone receptors (mPRs/PAQRs and PGRMCs), which are mediators of highly complex non-genomic progesterone actions with non-fully understood roles in cancer cells [85,86]. This evidence concerns the gene ESR1 and breast carcinoma.