In summary, the results of this study showed that SET overexpression is a recurrent molecular event that plays an oncogenic role in NSCLC, and inhibition of SET may provide an important therapeutic strategy for the treatment of NSCLC by targeting PP2A, and facilitate down-regulation of several PP2A-regulated targets including AKT and ERK kinase, p27, cyclin D1, and MMP9. This evidence concerns the gene MMP9 and non-small cell lung carcinoma.