We found pronounced interaction signals between different CAF subclusters and all three types of epithelial cells, among which high-malignant epithelial cells exhibited the most significant communication signals with the myofibroblastic CAFs1 (myCAFs1) and myCAFs2 subclusters, and FN1 and COL1A1 generated by CAFs played critical roles in this process, suggesting that the progression of UTUC may be attributed to the activation of tumor cells by CAFs. The gene discussed is TBX1; the disease is neoplasm.