In general, ERα can induce estrogen-dependent proliferation while ERβ can inhibit it, but the overall biologic effect of estrogenic compounds on different cells, tissues and tumour types is determined by the complex interplay of ER subtypes, isoforms, ER-related receptors and heterodimerization, presence of transcriptional coactivators and corepressors, as well as estrogen and non-estrogen mediated phosphorilation of all the above-listed ’players’. This evidence concerns the gene ESR2 and neoplasm.