However, knowing that several reports link STAT5a expression to tumor progression, and previous studies have demonstrated an inverted relationship of Cav-1 and STAT5a expression both in vitro and in vivo [26, 27], the current work focuses on the specific role (s) of STAT5a in early estrogen-stimulated BCa formation and progression, using both our established mouse model of estrogen-induced DCIS lesions in Cav-1 KO mice [28] and in vitro human DCIS cells with differing STAT5a expression levels. This evidence concerns the gene CAV1 and neoplasm.