Enrichment of cytotoxic Lin–CD7+CD127–CD56+CD45RO+ ILCs in mismatch-repair (MMR) deficit CRC tissues with tissue-resident (CD103+CD69+) phenotypesCorrelation of ILC with the infiltration of tumor-resident cytotoxic, helper and γδ T cells with highly similar activated (HLA-DR+CD38+PD-1+) phenotypesEnrichment of PD-1+ γδ T cells in MMR-deficient cancers and potential treatment via PD-1 checkpoint blockade. This evidence concerns the gene NCAM1 and neoplasm.