It may be a reasonable strategy that the YS110 treatment specifically induces internalization of both CD26 and Y-TR1 into the nucleus from the cell surface in cancer cells but not in normal CD26-positive cells, such as the endothelium or lymphocytes, and then, YS110 suppresses the POLR2A transcription, and TR-1 inhibits TFIIH and POLII, which leads to additive or synergistic anti-tumor effects [15,16]. Here, DPP4 is linked to neoplasm.