Some proinflammatory molecules, such as IFN-γ, tumor necrosis factor (TNF)-α and vascular endothelial growth factor (VEGF), promote the expression of the checkpoint protein programmed death-ligand 1 (PD-L1) that leads to T cell exhaustion [58], which is associated with the impairment of antitumor adaptive immune responses and, thus, favor tumor progression. Here, IFNG is linked to neoplasm.