As shown in Figure 2A, the expression levels of p-Erk1/2Thr202/Tyr204 (9/9, 100%), p-mTORSer2448 (and its downstream targets, p-4EBP1Thr37/46 and p-S6Ser235/236, 9/9, 100%), but not p-AktSer473 (1/9, 11.11%), were significantly upregulated in KTC mice compared with TC and KC mice, suggesting that the activation of the Mek/Erk/mTOR axis, but not PI3K/Akt/mTOR axis, is responsible for tumorigenesis in KTC mice. The gene discussed is AKT1; the disease is keratoconus.