For example, induction of neuronal MCP-1/CCL2 during mild impairment of oxidative metabolism caused by microglial recruitment/activation exacerbated neurodegeneration in thiamine-deficiency- (TD-) induced neuronal death, while CCL2-knockout (KO) mice were resistant to TD-induced neuronal death, suggesting that the chemokine CCL2 mediates microglial recruitment and neurodegeneration in this model [25]. This evidence concerns the gene CCL2 and hyperinsulinemic hypoglycemia, familial, 4.