In addition, dysfunctional CD8+T cells in the tumor microenvironment (TME) often upregulate inhibitory molecules including the T cell immunoglobulin and mucin domain (TIM-3) and programmed cell death protein 1 (PD-1) 41,42, to inhibit the magnitude of immune responses 43-48, while blocking such inhibitory signaling (such as TIM-3 signaling) is a promising strategy to rescue exhausted CD8+T cells for counter immunotherapy resistance 49-54. The gene discussed is HAVCR2; the disease is neoplasm.