Treatment of these cells with the p110δ-specific inhibitor IC87114, suppressed the constitutive Akt activation (Sujobert et al., 2005; Billottet et al., 2006) to equal levels as those observed upon the pan-PI3K inhibitor LY294002 treatment (Sujobert et al., 2005) confirming that the p110δ is the main isoform contributor of PI3K activity in AML cells. Here, PIK3CA is linked to acute myeloid leukemia.