AKT1 and hyperhomocysteinemia: Abekhoukh and colleagues demonstrated that in mice with hyperhomocysteinemia due to a genetically induced deficiency of the enzyme cystathionine beta synthase, a specific kinase termed dual-specificity tyrosine phosphorylation regulated kinase 1A modulated the PI3K/Akt pathway resulting in increased levels of phospho-Akt [34].