However, in conjunction with evidence that JAM-A may regulate HER2 expression [8] and that HER2 expression is proportionally higher in DCIS than invasive ductal carcinomas [30] or flags DCIS tumors that progress to invasive disease [14], the aim of this study was to explore the value of pharmacologically inhibiting JAM-A in HER2-positive breast DCIS models. Here, F11R is linked to ductal breast carcinoma in situ.