The anti-metastatic activity of NK cells is well established in several cancer types, but the mechanisms underlying NK cell metastasis infiltration and acquisition of anti-tumor characteristics remain unclear.  Herein, we investigated the cellular and molecular factors required to facilitate the generation of an ILC1-like CD49a⁺NK cell population within the liver metastasis (LM) environment of colorectal cancer (CRC). We show that CD49a⁺NK cells had the highest cytotoxic capacity among metastasis-infiltrating NK cells in the MC38 mouse model. Furthermore, the chemokine receptor CXCR3 promoted CD49a⁺NK cell accumulation and persistence in metastasis where NK cells co-localize with macrophages in CXCL9 and CXCL10 rich areas. By mining a published scRNA-seq dataset of a cohort of treatment-naïve CRC patients, we confirmed the accumulation of CXCR3⁺NK cells in metastatic samples, that correlated with better prognosis. Conditional deletion of Cxcr3 in NKp46⁺ cells and antibody-mediated depletion of metastasis-associated macrophages impaired CD49a⁺NK cell development, indicating that CXCR3 and macrophages contribute to efficient NK cell localization and polarization in LM. Conversely, CXCR3^neg NK cells maintained a CD49a^- phenotype in metastasis with reduced parenchymal infiltration and tumor killing capacity. Furthermore, CD49a⁺NK cell accumulation was impaired in an independent SL4-induced CRC metastasis model, which fails to accumulate CXCL9⁺ macrophages. Together, our results highlight a role for CXCR3/ligand axis in promoting macrophage-dependent NK cell accumulation and functional sustenance in CRC LM.