At the molecular level, chronic hyperinsulinemia induces serine/threonine phosphorylation of insulin receptor substrate (IRS) proteins via inflammatory kinases such as c-Jun N-terminal kinase (JNK) and IκB kinase β (IKKβ), thereby impairing downstream phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signalling [9]. This evidence concerns the gene AKT1 and hyperinsulinism.