The current investigations stemmed from observations that JAM-A and HER2 are co-expressed in breast cancer cells and patient tissues [3], that cleavage of overexpressed JAM-A may be a biomarker of resistance to HER2-targeted therapies in breast cancer patients [13], and that JAM-A acts as a novel transcription-level regulator of the HER2 family member HER3 in breast cancer settings [18]. This evidence concerns the gene F11R and breast carcinoma.