Interaction of LAG3 with its ligands i.e., MHC class II molecules, galectin-3, liver sinusoidal endothelial cell lectin (LSECtin), and fibrinogen-like protein 1 (FGL1) [20], mediates various signalings leading to impairment of TILs functions, including inhibition of Th1 proliferation and reduced production of interleukin-2 (IL-2), Interferon-γ, and tumor necrosis factor (TNF) in T cells, resulting in tumor escape [21]. This evidence concerns the gene LAG3 and neoplasm.