To further verify whether OM could inhibit TLR signaling, we employed the nuclear factor‐κB/activator protein 1 (NF‐κB/AP‐1) and interferon regulatory factor (IRF) reporter cell systems to evaluate the effects of OM on the two arms of TLR4 signaling, the myeloid differentiation factor 88 (MyD88)‐dependent and MyD88‐independent signaling pathways, respectively (Figure 3a). The gene discussed is TLR4; the disease is ocular melanoma.