Previous studies demonstrated that baicalin attenuated ER stress induced by tunicamycin through the CHOP/eNOS/NO pathway in cardiomyocytes and prevented lipotoxicity in AML-12 cells by reducing the interactions between TXNIP and the NLRP3 inflammasome [30–33]; here, we also showed this effect. The gene discussed is NLRP3; the disease is acute myeloid leukemia.