In addition, the inability of high BST-2 expressing MDA-MB-231 and SK-BR-3 cells to respond to DAC- or 5-AzaC-mediated induction of BST-2 expression suggests that high BST-2-expressing aggressive breast cancers at some point may have lost methylation-dependent regulation of BST-2 transcription which results in BST-2 overexpression and promotion of breast malignancy [4]. Here, BST2 is linked to breast cancer.