CTRL and neoplasm: Consistent with the hypothesis that Nucl-TAP transiently inhibits TAP mRNA and induces the expression of new antigens in tumor lesions, treatment of subcutaneously implanted palpable 4T1 tumor-bearing Balb/c mice with Nucl-TAP, but not with Nucl-Ctrl or Ctrl-TAP, inhibited tumor growth (Fig. 3a), and could be further enhanced by co-treatment with PD-1 Ab or Flt3 ligand (Fig. 3b), suggesting that increasing the antigenic burden of tumor cells by transient TAP downregulation could enhance the effectiveness of immune potentiating therapies, not limited to checkpoint blockade.