Early studies found that sustained T-cell activation induced by a chronic inflammatory environment, for example, during chronic viral infection or in a tumor, causes persistent LAG3 expression by T cells, which frequently coexpresses with other IRs such as PD1, TIM3, TIGIT, CD160, and 2B4, subsequently resulting in a dysfunctional T-cell state (73). This evidence concerns the gene CD160 and neoplasm.