Recent studies have reported that TXA2 demonstrates effects on promoting cancer cell proliferation,21, 22 and is also involved in post‐stroke–related neuronal cell damages.33 The success of engineering the active SCHEC, which specifically directed COX‐1–produced PGH2 to be passed to TXAS, was the first to make it possible to control cellular AA metabolism in favour to TXA2 and disfavouring other prostanoids. The gene discussed is TBXAS1; the disease is cancer.