One of the plausible mechanisms is that each estrogen receptor isoform (ER-α, ER-β, and G protein-coupled estrogen receptor) exhibits different roles in tumor growth and, therefore, it is possible that differential roles of estrogen receptor signaling could be due to different formation (proportion) of the estrogen receptor isoforms between hepatic and breast cancer cells. The gene discussed is ESR2; the disease is breast carcinoma.