Therefore, FAK inhibitor which could destroy stromal fibrosis might be a promising candidate in the treatment of KP tumor after its resistance to PD-1 blockade; (ii) Activated fibroblastic FAK was observed in KL tumors, however, how LKB1-deficiency KRAS-mutated tumor cells activated CAF and resulted in hyperactivating FAK pathway was not determined. This evidence concerns the gene PDCD1 and neoplasm.