While some literature data suggested that PD-1, LAG-3, and TIM-3 expressing T cells are exhausted and dysfunctional [43–45], others demonstrated that these immune checkpoints, in particular PD-1, are also upregulated following activation and effector T cell differentiation [46–48], and therefore expression per se does not reflect an exhausted status, rather these markers identify the autologous tumor-reactive repertoire infiltrating different tumors [46–49]. The gene discussed is LAG3; the disease is neoplasm.