However, it is known that TGF-β signaling activation in macrophages can lead to the polarization of macrophages to adopt a M2-like phenotype.22 In addition, it was previously demonstrated that the binding of integrin αV/β8 to GARP would lead to the release of latent TGF-β from GARP and subsequent activation of TGF-β.23 Thus, we hypothesized that the interaction between GARP/TGF-βRII and integrin αV/β8 could potentially serve as cell-surface mediators that confer tumor-macrophage interactions and subsequently activate TGF-β signaling that reprogram macrophages to adopt a M2-like phenotype. The gene discussed is TGFB1; the disease is neoplasm.