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). This evidence concerns the gene CXCL9 and neoplasm.