However, HK kinetic activity is inhibited when there is an increase in Adenosine diphosphate (ADP) concentration.[27] Furthermore, Aβ triggered detachment of HKI from neuronal mitochondria, contributing to oxidative stress and neurodegeneration in AD.[28] Recent research has shown that deletion of HKII in MG effectively promotes phagocytosis of Aβ plaques and mitigates cognitive impairment in 5xFAD AD mice.[29] The involvement of HK in COR‐modulated glycolysis remains uncertain. The gene discussed is HK2; the disease is Alzheimer disease.