Functionaly, STAT5a deletion in Cav-1 KO mice prevented mammary ductal branching and foci (DCIS-like lesion) formation, reduced the accumulation of PCNA positive epithelial cells, and maintained mammary ductal integrity by exhibiting both normal basement membrane and smooth muscle actin (myoepithelial) layer following estrogen treatment, suggesting that STAT5a could also play a role in invasion. This evidence concerns the gene STAT5A and ductal breast carcinoma in situ.