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. Here, UACA is linked to neoplasm.