Therefore, our investigation aimed to determine the potential relationship between I3A‐induced immunogenicity and these signaling pathways.[27, 28] Our findings revealed that co‐treatment with an Interferon α/β receptor (IFNAR) blocking antibody or NF‐κB pathway inhibitor BAY11‐7082 did not alter T cell activation by I3A‐treated tumor cells. The gene discussed is NFKB1; the disease is neoplasm.