As there is evidence for a functional redundancy between the PI3K isoforms, and, at least in a PTEN-deficient background, PI3Kα can compensate for the loss of PI3Kβ in solid tumors, we investigated the importance of PI3Kα signaling in DLBCL models resistant to AZD8186 [29–31]. This evidence concerns the gene PTEN and diffuse large B-cell lymphoma.