ESR1 and neoplasm: This could involve the direct genomic action of estrogen binding to nuclear estrogen receptors (ERα and/or ERβ), which then bind as dimers to estrogen-response elements (ERE) in the regulatory regions of estrogen-responsive genes in association with various basal transcription factors, coactivators, and corepressors to alter expression of genes involving in cell cycle control [1] and other tumor-promoting factors such as vascular endothelial growth factor [4].