Martin et al. observed that PD-L1 expression was upregulated in MET-amplified lung carcinoma cells upon IFNγ treatment, with this induction impaired by MET inhibition, suggesting an interaction between MET signaling and the JAK/STAT3 pathway downstream of IFNγ, leading to increased PD-L1 expression in tumors [30]. This evidence concerns the gene STAT3 and lung carcinoma.