For example, in addition to PI3Kδ, the related kinase PI3Kα has been implicated in signaling through the BCR in Activated B cell-like (ABC) DLBCL [16,17], providing a potential explanation for the greater clinical activity of the dual PI3Kα/δ inhibitor copanlisib compared to the PI3Kδ inhibitor idelalisib in patients with DLBCL [18,19]. This evidence concerns the gene BCR and diffuse large B-cell lymphoma.