Furthermore, suppression of leukemia cell growth in Jurkat cell-engrafted leukemic mice by either rapamycin or U0126 treatment or a combination of both further supports the importance of both the Raf-MEK-ERK and Akt-mTORC1 pathways in leukemia proliferation, especially since a combination of both inhibitors had an additive effect in vivo (Supplementary Fig. S6). The gene discussed is AKT1; the disease is leukemia.