Indeed, PI3K subunits play a key role in oncogenesis: somatic mutations in p110δ (causative for APDS1) have been found in locations analogous to oncogenic variants in p110α and in patients with non-APDS-related DLBCLs; furthermore, tumour-suppressor p85α mutations (causative for APDS2), leading to p110α hyperactivation, have been found in gliomas and colon, endometrial, and breast cancers (14, 29, 30). This evidence concerns the gene PIK3CD and activated PI3K-delta syndrome.