AKT1 and myeloid leukemia: PML (or pro-myelocytic leukemia), a tumor-suppressor protein enriched on the ER side of MAM microdomains, modulates Ca2+ ion release from IP3R by forming a multi-protein complex with the receptor, AKT (or protein kinase B), and protein phosphatase A, thereby modifying the ER-mitochondria Ca2+ ion transfer [158].