These results suggested that the inhibition of cell migration by Andrographolide was mainly due to the decreasing functional activity and/or downregulation of protein expression of NHE1, and that the activation of apoptotic pathway involved with Bcl-2, PARP, and Caspase 3 played a key role on the mechanism of Andrographolide-induced anti-cancer effect. Here, BCL2 is linked to cancer.