Several plausible explanations could be hypothesized, including a heterogeneous exhaustion/dysfunctional status of activated TILs (48, 49), varying TCR affinities (50), antigen concentration on the surface of autologous tumor cells (51), or the possibility that CD137+ TNF- IFNγ- TILs may be secreting other effector molecules. The gene discussed is TNF; the disease is neoplasm.