However, individual inhibition of AhR or c‐MYC did not affect the expression of the other protein, and dual knockdown of AhR and c‐MYC in tumor cells induced highest level of T cell activation, suggesting that AhR and c‐MYC downregulation may act in a complimentary rather than interdependent fashion to mediate I3A‐induced tumor immunogenicity. Here, MYC is linked to neoplasm.