Invariant natural killer T (iNKT) cell-derived interferon-gamma (IFNγ) plays a critical role in orchestrating effective antitumor immune responses. T cell production of IFNγ is often limited within tumors because it is highly dependent on glycolysis, which is scarce within nutrient-deprived tumor microenvironmnets (TMEs). However, it is not clear how such nutrient restriction affects iNKT cells. Here we investigated the metabolic strategies that enable human iNKT cells to sustain IFNγ production under metabolically challenging conditions. In contrast to conventional T cells, we found that glucose is dispensable for iNKT cell IFNγ production and that they can maintain IFNg production even during complete glucose deprivation by relying on mitochondrial metabolism of glutamine (glutaminolysis). Flow cytometric and extracellular flux analyses showed that iNKT cells have high basal levels of oxidative metabolism, which results in increased intracellular ATP levels, and ultimately leads to buildup of glycogen stores. We thus hypothesized that iNKT cells might be able to mobilize stored glycogen to support IFNγ production in nutrient-limited conditions. When exposed to tumor spheroids, iNKT cells, unlike conventional effector T cells, remained resistant to the metabolically challenging conditions created by the tumor cells and did not show any marked reduction in their ability to make IFNγ. Further studies using inhibitor of glycogenolysis or glycogen breakdown in the presence of tumor conditioned media confirmed a role for glycogen in supporting their IFNγ production in such nutrient-restricted environment. These findings highlight the distinct metabolic programming of iNKT cells and their capacity to remain functionally competent under hostile conditions. Our results underscore the potential of iNKT cells as metabolically resilient effectors for cancer immunotherapy, capable of overcoming limitations faced by conventional T cell-based treatments.