Because activation of the AT1-R by Ang II is upstream of STAT3, these data suggest that blockade of the AT1-R sensitizes NSCLC cells to STAT3 pathway inhibition and that a combination therapy consisting of a STAT3 pathway inhibitor and an AT1-R antagonist might represent a potential novel and alternative therapeutic approach for cancer treatment. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.