These mechanistic observations were further supported by human CRC organoid-based experiments, where TGFBI blockade improved expansion and tumor cell killing by major histocompatibility complex class I-restricted cytotoxic T cells.<h4>Conclusions</h4>Taken together, our data demonstrate that TGFBI acts as a sIC counter-regulating T cell activation, differentiation, and effector function, which can be restored by TGFBI blockade, with broad implications for novel immunotherapy strategies in solid tumors. This evidence concerns the gene TGFBI and colorectal carcinoma.