At early stages the effects on cell proliferation were predominant: tumors from rapamycin-treated mice had fewer GLI2A+ tumor cells and a striking absence of hyperproliferative GLI2A-negative epithelial cells (Figure 6), suggesting that both cell-autonomous effects of GLI2A in tumor cells and paracrine signals driving proliferation in neighboring gastric epithelium are dependent on mTOR signaling. Here, MTOR is linked to neoplasm.