Numerous COX-2 selective drugs have been shown in long-term research to increase cardiovascular morbidity. These negative effects of long-term COX-2 inhibition are mostly brought about by the general suppression of prostanoid production, which also causes a reduction in the release of tumor-promoting PGE2 and anti-thrombotic prostaglandins such PGI2. Selective inhibitors of PGE2, which are overexpressed in malignancies, could be more effective than COX inhibitors and result in a higher therapeutic advantage. The gene discussed is PTGS2; the disease is neoplasm.