The fact that LAG-3 contributes to the effector functions of T-cells is contradictory to its described role as a checkpoint molecule to be targeted in certain cancers.31–36 In view of our findings, it is reasonable to suppose that LAG-3 plays different roles depending on the activation status of the T-cells, enhancing effector functions on activated T-cells, while promoting suppressive features on Treg or exhausted T-cells. The gene discussed is LAG3; the disease is cancer.