Given that CREPT/RPRD1B promotes tumorigenesis by STAT3-driven gene transcription in p300-dependent manner [28], p300 augments the cell metastasis of HCC and NSCLC [31,32], and p300 overexpression is also proved in our detected NSCLC samples, whether p300 can acetylate STAT3 and affect its-Y705 phosphorylation, and the effect of the interaction between these two posttranslational modifications on MMP19 expression, cell migration and invasion in IL-17-stimulated NSCLC cells require to be ascertained. The gene discussed is IL17A; the disease is non-small cell lung carcinoma.