Consistent with established paradigms of COX-2 in cancer [6,35,36], deletion of MEC COX-2 delayed mammary tumor onset, lowered tumormultiplicity, reduced tumor cell proliferation and decreased tumor vascularization.Reduced vascularization in COX-2MECKO tumors was associated with lowerexpression of VEGFA and its receptor VEGFR2, a dominant pro-angiogenic pathway in tumors [37], consistent with the role of COX-2 in promoting the angiogenic switch thatallows tumors to progress [38]. This evidence concerns the gene KDR and breast cancer.