In addition, the DNA damage-induced apoptosis suppressor (DDIAS) has been reported to promote the progression of lung cancer through the regulation of the STAT3 pathway, and DDIAS inhibitors were found to suppress the activation of c-Jun NH(2)-terminal kinase (JNK) or interfere with DDIAS/STAT3 binding [68,69]. This evidence concerns the gene STAT3 and lung carcinoma.