The reasons remain to be determined, but could include differential effects of Itpkb inactivation, Akt activation, or PTEN loss on PI3K signaling in HSC, or, alternatively, a premature death of Itpkb−/− mice due to either anemia (26) or infections secondary to immunodeficiency (47) before blood cancer can develop. Here, AKT1 is linked to immunodeficiency disease.