It is well-established that tumor-reactive T cells undergo differentiation within the tumor, progressing from a progenitor-exhausted state (Ly108+TIM-3−, Texprog), which retains proliferative potential, through an intermediate-exhausted state (Ly108+TIM-3+, Texint) characterized by high effector function, and ultimately into a terminally exhausted state (Ly108−TIM-3+, Texterm) (Supplementary Fig. 1c) [13–15]. The gene discussed is HAVCR2; the disease is neoplasm.