We showed that this absence of IFNγ response in CRC, regardless of the microsatellite status, could not be accounted for by (1) a significant decrease in CD8+, Tbet+ TIL infiltrate, (2) the absence of IL-18Rα expression by those TILs, (3) the overexpression of the immune checkpoint PD1 as well as of other ICPs (personal observation), or (4) an increase in the main immunomodulatory cytokines (IL-10, TGFβ) in the tumor microenvironment. The gene discussed is TBX21; the disease is neoplasm.