When combined with an anti-PD1 (RMPI-14 clone, 250 μg/mouse), the α-CD163-dxr controlled tumor growth to the same extent observed without anti-PD1 treatment; furthermore, if the αCD163-dxr was replaced with the anti-PD1 therapy, tumors growth quickly resumed, suggesting that depletion of CD163+ M2-TAMs-induced tumor regression independently of the blockade of PD-1/PD-L1 [102]. Here, PDCD1 is linked to neoplasm.