It has been demonstrated that within the GCPs, during cerebellar development, Shh signaling differently regulates the downstream effectors of the mTOR pathway, thus promoting protein translation and increasing cell proliferation (89, 90); in turn, in tumor cells the mTOR/S6K1 pathway can directly activate Gli1, independently of the Shh/SMO pathway, which is also a cause of resistance of tumor cells to inhibitors targeting Shh/SMO signaling (91). The gene discussed is GLI1; the disease is neoplasm.