Background: The tumor microenvironment (TME) is a key determinant of progression and treatment response in gastrointestinal stromal tumors (GIST). Oncogenic KIT mutations in different exons (exon 9 vs exon 11) are clinically relevant, but their impact on immune and stromal architecture in situ remains insufficiently understood. We hypothesized that KIT exon 9 and exon 11 mutations drive distinct spatial transcriptional programs and immune cell compositions. Methods: FFPE samples from KIT‑mutated GIST (exon 9 and exon 11) were profiled using the NanoString GeoMx® Whole Transcriptome Atlas (18,695 protein‑coding genes). Eleven areas of illumination per case were selected in tumor and peritumoral regions and segmented into CD45⁺ (immune‑enriched) and CD45⁻ (tumor/stromal) compartments. Cell‑type abundances in CD45⁺ segments were estimated with SpatialDecon. In parallel, three multiplex immunofluorescence (mIF) panels (DOG1/CD11c/CD11b/CD68/CD45/HLA‑DR; DOG1/CD45RO/CD56/CD4/CD8/CD20; DOG1/CD45/CD16/CD56) were applied to independent retrospective GIST cohorts (n=170), and cell densities were quantified in tumor and stromal compartments using QuPath‑based segmentation and FACS‑like phenotyping. Results: GeoMx analysis identified 2315 differentially expressed genes in CD45⁺ tumor regions between exon 9 and exon 11 tumors, indicating exon‑specific immune transcriptional programs. SpatialDecon deconvolution revealed that exon 11-mutant tumors exhibited higher NK‑cell scores (adjusted p≈6×10⁻⁶), whereas exon 9-mutant tumors showed higher fibroblast (adjusted p≈6×10⁻⁶) and CD8⁺ memory T‑cell signals (adjusted p≈1.9×10⁻⁴). In the large mIF cohorts, unsupervised analyses of DOG1‑gated tumor regions confirmed robust technical performance of all three panels and demonstrated genotype‑segregated TME patterns KIT-mutant cases, and within them exon 9 vs exon 11 tumors, occupied distinct regions in PCA space, with exon 11 tumors showing higher CD56⁺ (NK/NKT) and myeloid (CD11b⁺/CD68⁺/HLA-DR⁺) densities, whereas CD8⁺CD45RO⁺ memory T cells were more abundant in exon 9 tumors, independently of PDGFRA-mutant GIST. Across panels, these phenotypic differences aligned with the GeoMx‑derived enrichment of NK cells in exon 11 tumors and of and CD8⁺ memory T cells in exon 9 tumors. Conclusions: Integrated spatial transcriptomics and multiplex IF demonstrate that KIT exon 9 and exon 11 mutations are associated with distinct immune and stromal microenvironments in GIST, characterized by an NK‑cell-enriched, myeloid cells , less fibroblast‑ and CD8⁺ memory T‑cell-dense niche in exon 11 tumors and the converse pattern in exon 9 tumors. These data support the concept that the precise KIT exon mutated imprints the TME and should be considered when designing genotype‑adapted combinations of kinase inhibition and immunotherapy.