It effectuates tumor cell apoptosis through the activation of the JNK/c-Jun and JNK/SAPK pathways, leading to reduced Bcl-2 levels and elevated Bax, as well as activated Caspase-3 and PARP in oral cancer (YD10B and Ca9-22) and pancreatic cancer (SW1990) cells [922, 923]. This evidence concerns the gene BAX and neoplasm.