The hyperinsulinemia resulting state is thus capable of inducing serine/threonine phosphorylation of insulin receptor substrate (IRS), which is prone to promote IRS degradation and block the phosphorylation of tyrosine, which represents a key stage of continuing the remaining phosphorylation cascades of downstream targets, either phosphatidylinositide 3-kinases (PI3K) or a class of small GTPase (RAS) involved in PI3K/ protein kinase B (Akt)/ Forkhead box transcription factors of the class O (FOXO1) signaling pathways [14]. This evidence concerns the gene AKT1 and hyperinsulinism.