This model could also be applied to humans, based on the following considerations—(1) the human PDXK gene inserted in dPdxk1 mutant flies is capable of reducing hyperglycemia, CABs, and AGE accumulation [45]; (2) RNAi-induced silencing of the human PDXK gene produces CABs in fibroblasts and HeLa cells, as well as 4-DP treatment in mock cells [45]; (3) alpha-lipoic acid treatment rescued DNA damage induced by PDXK depletion [45]; (4) the expression in the dPdxk1 mutant flies of 4 PDXK human variants with reduced or impaired catalytic activity did not rescue CABs nor AGEs [53]. The gene discussed is PDXK; the disease is Hyperglycemia.