Amplified in breast cancer 1 (AIB1 or SRC-3) is a human cancer-overexpressed coactivator for transcription. In mice, overexpression of AIB1 has caused high incidence of mammary adenocarcinoma, and inactivation of AIB1 has suppressed mammary tumorigenesis induced by the ras oncoprotein. However, the exact role of AIB1 in mammary epithelium and in determination of the susceptibility of mammary gland to chemical carcinogen has remained elusive. The authors have performed mammary epithelial transplantation and 7,12-dimethyl-benz(a)anthracene (DMBA)-induced mammary carcinogenesis in wild type (WT) and AIB1 mutant mice to approach these problems. The cover figure shows the defective outgrowth of mammary ducts from the transplanted AIB1^-/- mammary epithelium (right upper and middle panels) compared with the transplanted WT (left upper panel) and AIB1^+/- (left middle panel) mammary epithelium in WT recipient mice, the positive X-gal staining of mammary ducts emanating from the transplanted AIB1^+/- (left middle panel) and AIB1^-/- mammary epithelium (right middle panel), and the comparable outgrowth of mammary ducts from WT (left lower panel) and AIB1^-/- (right lower panel) mammary epithelium in WT recipient mice stimulated with a pituitary isograft. The cover figure also shows the reduction of incidence and the extension of latency of DMBA-induced mammary tumorigenesis in AIB1^-/- mice compared with AIB1^+/- and WT mice (inset). The data demonstrate that the role of AIB1 in mammary ductal growth is an epithelial autonomous function and the lack of AIB1 function can be compensated by enhanced hormonal stimulation. Importantly, inactivation of AIB1 makes the mammary gland more resistant to chemical carcinogen-induced tumorigenesis. For details, see the article by Kuang et al. on page 7993 of this issue.