BAX and laryngeal carcinoma: Previous studies demonstrated that baicalein was capable of up-regulating the expression of Bax, reducing the expression of Bcl-2, and elevating the ratio of Bax/Bcl-2, decreasing mitochondrial transmembrane potential as well as triggering the release of Cyto-C into the cytoplasm, which in turn formed apoptotic vesicles with activated caspase-9 and apoptotic protease activating factor-1 (Apaf-1), thereby activating caspase-3 and the subsequent mitochondrial apoptotic pathway in human laryngeal carcinoma Hep-2 cells [15].