Evidence suggests that dysregulated tumor-intrinsic pathways, such as the PI3K/mTOR, Wnt/β-catenin, and AXL signaling pathways, might play a key role in ICB resistance by endorsing the expression of an immunosuppressive cytokine profile and facilitating the trafficking of immunosuppressive cell populations to the TME of uLMS. This evidence concerns the gene MTOR and neoplasm.