ER-α activates the extracellular signal-related kinases (ERKs)/mitogen-activated protein kinases (MAPK), phosphatidylinositol-3-kinase/protein kinase B (Akt) signalling pathways, which promote cell growth, whereas ER-β triggers apoptosis in tumour cells via caspase 3 activation, phosphorylation of p38/MAPK and PARP cleavage, blocks the cell cycle by increasing the expression of the oncosopressors p21 and p27 and decreasing that of the protooncogenes c-myc and cyclins [14,15]. The gene discussed is ESR1; the disease is neoplasm.