The development of traditional molecular meningioma therapies targeting genetic variants has not produced satisfactory results.[5, 24, 36] Triclosan significantly inhibited the proliferation of tumor cells in SULT1E1+ MOs, however its clinical application for the treatment of high‐grade meningioma is limited by the potential oncogenic risks.[37] Here, we present another potential therapeutic strategy that effectively inhibits the SULT1E1+ subpopulation. The gene discussed is SULT1E1; the disease is neoplasm.