These data suggested that tumors growing in the liver hampered the efficacy of PD‐1 blockade to tumors developed in other organs (i.e. SubQ in our study), similar to the reduced immunotherapy efficacy in melanoma and NSCLC patients with liver metastasis.[7, 8] Such observations supported that this model could be used to dissect the immune mechanisms of ICB resistance in liver metastasized CRC patients, while our models could only study the impact of the cooccurrence of liver tumor on the efficacy of PD‐1 blockade tumors in other organs but not de novo liver metastasis. This evidence concerns the gene PDCD1 and non-small cell lung carcinoma.