Mice deficient for PI3Kδ develop leukemia significantly faster. (A) Kaplan-Meier plot of PI3Kδ^+/− and PI3Kδ^−/− recipient animals after injection of wt v-abl–transformed cells. PI3Kδ^−/− recipient mice developed disease significantly earlier when compared with their PI3Kδ^+/− littermate controls (log-rank test; P = .003; n = 7 for each group; 3 independently derived cell lines were injected). (B) Kaplan-Meier plot of PI3Kδ^+/− and PI3Kδ^−/− recipients on a RAG2^−/− background after injection of wt v-abl–transformed cells. Again, PI3Kδ^−/− recipients succumbed significantly earlier to disease than PI3Kδ^+/− littermate controls (log-rank test; P = .007; n = 4 for each group). (C) Kaplan-Meier plot of 10 PI3Kδ^+/− and 10 PI3Kδ^−/− recipient animals after injection of wt v-abl–transformed cells. A total of 5 animals of each group received anti-NK1.1 antibody to deplete NK cells (dashed lines). In the absence of NK-cell depletion, PI3Kδ^−/− recipient mice again developed disease significantly earlier when compared with their PI3Kδ^+/− littermate controls (solid lines; log-rank test; P = .03). This difference was lost upon NK-cell depletion (dashed lines; log-rank test; P = .61; n = 5 for each group).