IFNG and neoplasm: Canonically, PD-L1 interacts with its receptor PD-1 on tumor-specific T cells and limits their antitumor activity.23 Anti-PD-L1 therapy blocks this interaction, thereby reinvigorating T cell proliferation and effector functions such as IFN-γ secretion.24 However, like anti-PD-1, PD-L1 blockade can also directly and indirectly modulate myeloid cell function.