The fact that, in parallel to the upregulation of MHC class I molecules in the IL-6-deficient host milieu, a concomitant increase in PD-L1 expression was observed on the surface of IL-6-proficient CT26 tumor cells [91], implied that the therapeutic blockade of IL-6 signaling can potentially improve the responsiveness of CRC patients to checkpoint inhibitor therapies. This evidence concerns the gene IL6 and colorectal carcinoma.