Similarly, the PD‐L1 level was also decreased in AOM/DSS‐induced primary colorectal tumors in SRC‐1−/− mice (Figure 1I), whose tumor burden was lower than that of SRC‐1+/+ mice.[16] Taken together, these results suggest that SRC‐1 may promote CRC immune escape by elevating PD‐L1 levels, thereby contributing to CRC progression. Here, SRC is linked to colorectal neoplasm.