In melanoma, collagen mediates CD8 + T cell exhaustion through LAIR1/Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP1) pathway while combination of programmed death 1 (PD-1) blockades with overexpression of LAIR2, a soluble homologue of LAIR-1 with higher affinity for collagen and thereby acts as a decoy receptor, significantly overcome tumor growth and lung metastasis [491, 492]. This evidence concerns the gene LAIR1 and neoplasm.