We also found that in the presence of hyperglycemia and hyperlipidemia, probably, in part, via increasing the endogenous NOSi SDMA, UCAO alone, without L-NAME administration, induced infarction in C57BL/6 mice and ApoE-/- mice far more frequently (22.4% and 31.0%, respectively) than in naïve C57BL/6 mice (~2%). This evidence concerns the gene APOE and infarction.