Because ER location regulates the estradiol signaling output, specific targeting of the interaction between estrogen receptors and signaling effectors (like Src family tyrosine kinases involved in signaling transduction pathways) or nuclear export receptors (exportin/Crm1 protein involved in ER export form nuclei) antagonizes the proliferative rate of breast cancer cells [3,4]. The gene discussed is ESR1; the disease is breast carcinoma.