AKT1 and atherosclerosis: Notably, although global deletion of Akt1 resulted in a much more dramatic disease phenotype characterized by cardiac dysfunction resulting from large ischemic LV infarcts (presumably from ruptured plaques), targeted deletion of Akt1 in VSMCs resulted in a relatively modest phenotype, suggesting that Akt1 loss in endothelial cells serve as the primary driver of the increased atherosclerosis observed in mice lacking Akt1 [11, 13].