Particularly, the high affinity interaction of Fibrinogen-like protein 1 (FGL1) and LAG-3 has revealed a major immune-evasion mechanism suppressing T cell anti-tumor responses and may constitute an important targetable pathway in cancer immunotherapy.115 A comprehensive appreciation of the receptor-ligand interactions and their biology remains essential for an optimal therapeutic targeting in clinic. Here, FGL1 is linked to neoplasm.