Collectively, these results suggest that I3A treatment downregulated AhR expression, increased JAK2 and STAT3 phosphorylation, and enhanced the expression of MHC‐I molecules, ultimately improving tumor immunogenicity. Furthermore, tumor cells with reduced AhR expression were found to be more immunogenic, and the use of AhR inhibitors prevented I3A‐induced degradation of AhR and subsequent enhancement of tumor immunogenicity. Here, STAT3 is linked to neoplasm.