In conclusion, our data provided evidence for the first time that STM inhibits growth and induces oxidative stress, which results in NF-κB inhibition, Bcl-2 family protein modulation, MMP dissipation, caspase-3 activation, and PARP cleavage, ultimately leading to mitochondrial apoptosis in A549 lung adenocarcinoma cells. The gene discussed is BCL2; the disease is lung adenocarcinoma.