CAFs from pancreatic cancer were described to express the somatostatin receptor sst1, whose activation using an sst1 agonist (SOM230, pasireotide) inhibited the mTOR protein synthesis pathway in CAFs, thereby dramatically decreasing the secretion of pro-tumor secreted proteins, including IL-6, inhibiting tumor growth and metastasis, and restoring chemosensitivity in preclinical mouse models including PDX [229,230]. The gene discussed is MTOR; the disease is neoplasm.