As shown in Fig. 3b, f, combination of TAP inhibition with checkpoint blockade using PD-1 Ab and/or recruiting DC to the tumor by treatment with Flt3 ligand, further potentiated the antitumor response, suggesting that increasing the antigenicity of tumor cells in situ by transient TAP downregulation could enhance the effectiveness of any immune-potentiating therapy, including but not limited to checkpoint blockade. Here, FLT3LG is linked to neoplasm.