Adoptive therapies using CAR-expressing natural killer (NK)-cells, a subset of cytotoxic lymphocytes, have demonstrated efficacy against B cell malignancies. However, the potential of engineered NK-cells against solid tumours remains unclear, with homing to tissues representing a limitation. All-trans retinoic acid (ATRA) and calcitriol (CAL) promote the establishment of tissue-resident T-cells that home towards either gut or skin, respectively, but if ATRA or CAL can boost NK-cell tumour infiltration and tissue-residency has not been investigated. We show that ATRA and CAL inhibit differentiation of human NK cells from umbilical cord blood haematopoietic stem cells in vitro, without impacting their tissue homing receptor expression patterns. However, ATRA and to a lesser extent CAL, promoted expression of tissue-homing receptors, including integrin β7, CLA, CCR10, CD49a, and CD69, on mature blood-derived NK-cell subsets, most potently in CD56^bright NK-cells and least in adaptive CD56^dim NK-cells. Compared to human blood CD8⁺ T-cells, CD49a and CLA were more strongly induced on NK-cells, whereas CCR9 and CCR10 were preferentially expressed by T-cells. In terms of NK-cell function, ATRA increased degranulation but decreased IFN-γ production. Altogether, this study provides evidence for ATRA and CAL modulating the homing phenotype of circulating NK-cell subsets, indicating a role in promoting tissue-residency. We provide insights on the distinct regulation of tissue-residency between innate and adaptive cytotoxic lymphocytes with potential implications for development immunotherapeutic strategies for solid tumours.