Specifically, Galectin-3 reduces IFN-γ diffusion through the tumor matrix avoiding the production of an IFN-γ–induced chemokine (such as CXCL9) required for T cell recruitment (45) and interacts with Galectin-3 binding protein from extracellular vesicles to suppress the activation of CD4, CD8, and CD56 effector cells through CD45 receptor, further promoting tumor escape (46). The gene discussed is LGALS3; the disease is neoplasm.