[8–14] Upon the action of PI3K converting phosphatidylinositol 4,5-bisphosphate into phosphatidylinositol 3,4,5-trisphosphate (PIP3), Akt, the pivotal molecule in the pathway, is activated as PIP3 binds to its pleckstrin homology domain, prompting a conformational change that exposes the Ser473 and Thr308 sites, which are then phosphorylated by phosphoinositide-dependent kinase 1 (PDK1) at Thr308 and PDK2 at Ser473, ultimately regulating cardiac recovery following myocardial infarction (MI) through the downstream signaling cascade. The gene discussed is PLEK; the disease is myocardial infarction.