Type 1 innate lymphoid cells (ILC1s) display tissue residency properties and unique tissue distribution. The liver is particularly enriched with ILC1s, while the mechansims regulating liver ILC1 maintenance and functions are poorly understood. In this study, we found high expression of the E3 ubiquitin-ligase enzyme ASB2 in liver ILC1s. Mice with conditional ablation of Asb2 in NKp46⁺ cells had decreased ILC1s in the liver but normal numbers of cNK cells. ASB2 deficiency had no impact on the proliferation and effector functions of ILC1s, but resulted in increased ILC1 apoptosis. Proteomic and RNA sequencing analysis revealed that signaling pathways related to fatty acid metabolism were enhanced in ASB2-deficient ILC1s. Increased lipid storage was observed in ASB2-deficient ILC1s and inhibition of lipid synthesis prevented the apoptosis of Asb2-deficient ILC1s. Using a murine model of colorectal cancer liver metastases, we found that ASB2 conditional deficiency resulted in more aggressive liver tumor progression. Consequently, Inhibition of lipid accumulation efficiently limited liver metastases and promoted ILC1-mediated anti-tumor immunity. Thus, our study uncovers lipid metabolism regulated by ASB2 as a gatekeeper for ILC1 maintenance and tumorcidal activities, providing insights into new therapeutic strategies against liver cancer.