Besides, an intriguing increase in expression of SHIP1 (Src homology 2-containing inositol-5′-phosphatase 1, that can enable inactivation of the PI3K-AKT signaling pathway) was observed in Nrf1α−/−-derived tumor, albeit it was almost unaltered in the initially-inoculated Nrf1α−/− cells, when compared with the wild-type controls (Figures 7(d) D7 and ). The gene discussed is AKT1; the disease is neoplasm.