Previous researches have revealed STAT3 can subject to phosphorylation (e.g., p-STAT3 at Ser727 or Tyr705) and acetylation, and its phosphorylation or acetylation is necessary for STAT3 activation promoting cancer tumorigenesis or metastasis and STAT3-driven gene transcription in the microglia and other cancers [23,27,28], but the role of STAT3 acetylation and the interaction of STAT3 acetylation and phosphorylation in MMP19 expression as well as NSCLC cell metastasis in response to IL-17 remain undefined. This evidence concerns the gene MMP19 and non-small cell lung carcinoma.