A recent report showed that cDC1 accumulation in transplantable mouse tumors depends on tumor-infiltrating NK cells secreting the chemoattractants CCL5 and XCL1, whereas disruption of this mechanism resulted in cancer immune evasion.11 Additionally, in certain human cancers, patient survival correlates with the transcript level of CCL5 and XCL1, which were also positively associated with the abundance of cDC1-like DCs expressing CLEC9A, XCR1, CLNK and BATF3, highlighting the clinical relevance of the findings. This evidence concerns the gene CLEC9A and neoplasm.