AKT1 and cancer: Considering these findings and the observed decrease in p-p85α (Tyr 508)–p110α complex formation causing the association of p85α with unphosphorylated PTEN at the plasma membrane after treatment with citrate, it is logical to suggest that the stabilization of p-p85α (Tyr 508)–p110 complexes at the plasma membrane has physiological relevance related to the promotion of Akt activation to allow the progression of the cancer cell proliferation cycle in aerobic glycolytic metabolism.