Invariant Natural Killer T (iNKT) cells are a unique subset of T cells with semi-invariant T cell receptors (TCR) and natural killer (NK) markers. They respond to glycolipid antigens presented by CD1d, and like T helper cells, differentiate into subtypes such as iNKT1, iNKT2, and iNKT17. iNKTs play a key role in both immune response and tissue homeostasis by rapidly releasing cytokines in response to pathological signals. Despite their known functions in various diseases, their role in hematological malignancies remains poorly understood. Clonal Hematopoiesis of Indeterminate Potential (CHIP) is a premalignant condition marked by somatic mutations in blood stem cells, leading to clonal expansion. Loss of the epigenetic modifier TET2 in CHIP results in myeloid skewing and increased inflammation, but those environmental impacts on iNKT survival and function have not been explored. In this study, we demonstrate that iNKT cells are reduced in the spleens of CHIP chimeric mice, suggesting impaired iNKT survival among the non-mutated cells. Transcriptomic analysis combined with studies of the chromatin landscape reveals NFkB activation and a differentiation bias towards iNKT17. Flow cytometry further confirms this perturbation, which may contribute to the overall pathogenesis of myeloid malignancies. Serum profiling of CHIP mice identified IL-6 as a potential driver of altered iNKT cell polarization. Interesting studies of distinct glycolipids, the antigens driving iNKT function, expressed uniquely in the mutant cells, are underway. Given their potential for use in allogeneic cell therapies, understanding the mechanisms underlying iNKT dysfunction in CHIP could enable the development of novel immunotherapeutic strategies to enhance cytotoxic activity and improve therapeutic outcomes.