Mutations in genes (PTEN, PI3KCD, PI3KR1) associated with the PI3K/AKT/mTOR kinase pathway that lead to increased AKT phosphorylation and subsequently increased S6 kinase activity produce a clinical phenotype (activated PI3-kinase delta syndrome– APDS) that includes increased susceptibility to viral infection, lymphoma, hypogammaglobulinemia, and lymphoproliferation [5–8]. Here, AKT1 is linked to agammaglobulinemia.