This hypothesis was supported by our demonstration that (1) TILs isolated from CRC, mostly CD4+ and half of the CD8+ subset, expressed IL-18 receptors, and (2) IL-18 stimulation significantly improved the basal IFNγ production of TILs, an increase correlated with the IL-18R expression level and occurring without T cell receptor (TCR) activation. Here, IL18R1 is linked to colorectal carcinoma.