We found that EP4 is an ideal therapeutic target to replace COX-2 for three reasons: (1) it accounts for most of the COX-2 mediated events in breast cancer progression; (2) it is relatively redundant for most physiological functions of COX-2 shared by EP2 via cAMP/PKA pathway; (3) it does not bind to cardio-protective prostanoid PGI215, depleted by COX-2 inhibitors. This evidence concerns the gene PTGS2 and breast carcinoma.