STAT3 and neoplasm: Both apigenin and luteolin (from 10 to 50 μM) inhibited STAT1 and STAT3 phosphorylation and decreased expression of STAT-dependent programmed death-ligand 1 (PD-L1), a major factor responsible for the suppression of the adaptive anti-tumor immune response in NSCLC and melanoma cell lines [207,208].