JNK contributes to immune evasion via PD-L1 expression by modulating the activity of c-Jun, an inducible transcription factor that directs gene expression changes such as PD-L1, a mechanism observed in melanoma (35); or via TLR4 (toll-like receptor 4) signaling as in bladder cancer (36) (Figure 1). The gene discussed is TLR4; the disease is melanoma.