Overexpression of proinflammatory transcription factors NF-κB, STAT3, and AP-1 results in the release of cytokines and chemokines, and pre-existing inflammation plays a critical role in immunosuppression via the STAT3 pathway, which stimulates the expression of programmed death ligands 1 and 2 (PD-L1 and PD-L2) in cancer cells and suppresses the activity of immune cells [93]. This evidence concerns the gene STAT3 and cancer.