The results of this study depict that FYN phosphorylates human COX2 on Tyr 446 and that the corresponding phosphorylated COX2 activating mutation promotes COX2 activity, and the phosphorylation inactivating mutation prevents the FYN-mediated increase in COX2 activity, which is known to be overexpressed in prostate cancer [182]. This evidence concerns the gene PTGS2 and prostate carcinoma.