Consistently, we observed upregulated expression of TME-associated genes involved in inflammation, angiogenesis, and extracellular matrix (ECM) remodeling, all of which contribute to metastasis by modulating stromal cell activity and altering the ECM.70,71 Given the crucial role of TME in tumor progression, our findings suggest that the pseudohypoxic state induced by CypD inhibition not only enhances the intrinsic metastatic potential of cancer cells but also reprograms the TME, creating a more permissive environment for tumor dissemination. The gene discussed is PPIF; the disease is neoplasm.