In the non-small cell lung cancer (NSCLC) cells and H460 xenograft tumor model, the apoptosis-inducing effects of ginsenoside Rk3 were triggered by mitochondria-dependent pathways, in which Rk3 decreased Bcl-2 expression, increased Bax expression, caused cytochrome c release, induced caspases 3, 8, and 9 activation, and promoted mitochondrial membrane potential changes [67]. This evidence concerns the gene CASP3 and neoplasm.