Natural killer (NK) cells are important for innate immune protection against cancer through direct killing of malignant cells and production of immunoregulatory cytokines, and hence one of the key targets in immunotherapies. In cancers, NK cells often become dysfunctional, and various factors are implicated in this process. Energy metabolism regulates immune cell function and it is becoming increasingly recognised that the tumour environment alters immune cell responses through changing nutrient availability. The extent to which the tumour environment interrupts NK cell metabolism to culminate in functional alterations remains to be investigated. In blood cancers, where tumour cells and immune cells share the same niches, tumour cells can disrupt NK cell metabolism, suppressing anti-tumor activity. We found that the metabolic signatures of NK cells are distinct from other lymphocyte populations, with higher lipid metabolism compared with that of B cells, ab T,  gd T and NKT cells. In mice with c-myc-driven B cell lymphomas, NK cells exhibited metabolic, developmental, survival, and functional defects, shown by decreased mitochondrial metabolism, abnormal mature NK subset compositions, increased apoptosis upon activation, and persistent suppression of IFN-g, respectively. Lymphoma-derived NK cells displayed increased lipid transcriptome, associated with increased lipid storage and higher propensity for lipid uptake compared with NK cells derived from healthy mice. We observed elevated circulating fatty acids in the lymphoma environment, and hypothesized that increased exposure to these systemic lipids drove the metabolic and functional alterations of NK cells. Conditioning NK cells in vitro with FA levels reminiscent of levels in the lymphoma environment mimicked tumour-induced NK cell dysfunction. This study identified lipid metabolism as one of major regulators of NK cell function which blood cancers manipulate to suppress NK cell effector responses. Current work aims to target PPARg, an identified regulator of lipid metabolism of NK cells to boost anti-tumour immunity.