In A549 and H1299 cells, cell proliferation was inhibited by artesunate, artemisinin and dihydroartemisinin via cell cycle arrest in the G1 phase.Also, apoptosis was induced by dihydroartemisinin in A549 cells (77, 78).In ABT-263 NSCLC cells with EGFR or Ras mutations, dihydroartemisinin inhibited STAT3 phosphorylation and activation, lowering surviving levels (79). This evidence concerns the gene STAT3 and non-small cell lung carcinoma.