UA exhibited a strong apoptotic activity against non-small cell lung cancer; it dow-regulated the expression of the JAK2/STAT3 pathway and reduced the expression of VEGF and PDL-1, hence hampering the STAT3/PD-L1 complex formation and the EGFR/JAFK2/STAT3 signaling pathways. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.