Upon phosphorylation, IRF3 translocates to the nucleus, where it activates the transcription of type 1 IFNs and ISGs, which is a hallmark of activation of the STING pathway.[31] Our immunohistochemical analysis of tumor tissues demonstrated elevated nuclear IRF3 expression in the C5‐PE38 treatment group (Figure 6i), indicating that the downstream of STING pathway was initiated. The gene discussed is IRF3; the disease is neoplasm.